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Inflammaging and cardiovascular disease: management by medicinal plants.

ABSTRACT

Background: In aging, a host of molecular and cellular changes occur which accelerate alteration and progression of inflammatory diseases. These conditions in the elderly people cause appearance of a phenomenon which has been denoted as "inflammaging". Understanding the pathogenesis and finding new methods for management of inflammaging are essential.

Purpose: In this paper we tried not only to explain inflammaging and its treatments with concentrating on medical plants but to collect a sufficient collection of anti-inflammatory plants with focusing on their mechanism of action.

Method: In this review paper, by searching in indexing cites, desired articles were obtained since 1995 by using keywords of inflammation, inflammaging, inflammation pathophysiology, free radicals and inflammation, aging inflammation, inflammatory disease, and plants or herbal medicine in inflammation.

Sections: In advanced age the generation of free radicals increases in cardiovascular system. Pathological inflammation is also associated with production of excess free radicals More importantly, chronic inflammation makes aged people susceptible to age-related diseases. Some medicinal plants have been shown promising results in inhibition of inflammaging. Some other sections such as inflammation and inflammaging in cardiovascular diseases, oxidative stress in cardiovascular complications, prevention and treatment strategies are presented.

Conclusion: The results of published papers show that the symptoms of several inflammatory diseases can be inhibited or treated by active ingredients from medicinal plants.

Keywords:

Aging

Anti-inflammatory drugs

Cardiovascular disease

Inflammation

Inflammaging

Medicinal plants

Introduction

The world's population age is increasing and the aging population is a risk factor for cardiovascular diseases (CVD). Aging generally causes some changes which, even in absence of usual risk factors, render the cardiovascular system prone to some diseases (Lakatta 2000).

The progressive degeneration of the heart in elderly makes it more vulnerable to stress and causes an increase in cardiovascular morbidity and mortality (Brodsky et al. 2004). Cardiovascular diseases are also fuelled by some other risk factors such as diabetes (Baradaran et al. 2013; Behradmanesh et al. 2013), hypertension (Asgary et al. 2013; Ghorbani et al. 2013), and obesity (Nasri and rafieian-kopaei 2013; Rabiei et al. 2013a; Favarato et al. 2014). Aging is a phenomenon resulted from genetic, epigenetic stochastic, and environmental events in different cells and tissues. In fact in aging, a host of molecular and cellular changes occur which accelerate these alterations and implicate in the progression of arterial diseases (Rabiei et al. 2013b; Favarato et al. 2014). Pathological inflammation is also associated with production of excess free radicals arising predominantly from mitochondria (Beller 2010; Rafieiankopaei et al. 2012). There are also evidences showing that in advanced age the generation of free radicals increase in cardiovascular system (Judge et al. 2005; Asadbeigi et al. 2014). More importantly, chronic inflammation makes aged people susceptible to age-related diseases (Franceschi et al. 2000).

A wide variety of diseases including diabetes (Asadbeigi et al. 2014) cancer (Azadmehr et al. 2011; Nasri and rafieian-kopaei 2014), infection (Bagheri 2013; Bagheri 2013), atherosclerosis (Rafieian-Kopaei et al. 2011; Rafieian-Kopaei et al. 2014a), cardiovascular diseases (Khosravi-Boroujeni et al., 2013; Sarrafzadegan et al. 2013), Alzheimer (Rabiei et al. 2013c, 2014) and other degenerative diseases (Mardani et al. 2014; Rafieian-Kopaei et al. 2014b) are associated with increased oxidative stress and inflammatory conditions and are degraded in aging. Moreover, the process of inflammation is involved in initiation and development of a wide variety of chronic diseases (Paolisso et al. 1998).

In aging the normal balance between the oxidative stress and antioxidant system culminates in cardiovascular complications. These conditions in the elderly people cause appearance of a phenomenon which has been denoted as "inflammaging". In fact, the word inflammaging is used to show inflammatory state in the aged individuals (Franceschi et al. 2000).

Chronic inflammation in aging tissues "inflammaging" is a pervasive feature of aging and most age-related diseases are associated with inflammation, in fact inflammaging is described as systemic, low-grade chronic inflammation in aged people, in absence of infection. It is a great risk factor for mortality and morbidity in the elderly people (Zhang et al. 2010).

A mild inflammation is predictive of, and is associated with many aging phenotypes. The etiology of inflammation in aging people and its contribution in adverse health events is unknown. The pathways that make us able to control inflammation are not fully established. Hence, understanding the pathogenesis and finding new methods for management of inflammation are beneficial. This paper, therefore, aimed to present the recently published papers regarding inflammation in cardiovascular diseases, focusing on the role of oxidative stress, and to summarize the herbal medicines which have had promising results in prevention and treatment of this phenomenon.

Inflammation and cardiovascular disease

Inflammation participates to the pathophysiology of a wide variety of chronic diseases particularly injury and infectious diseases. Interaction of various cells in the adaptive and innate immune systems with inflammatory mediators modulates the acute and chronic inflammation causing various diseases. This coordination in inflammatory mechanisms triggers remodeling of the extracellular matrix, oxidative stress, tissue injury, angiogenesis and fibrosis in various tissues. These inflammatory mechanisms are involved in most of cardiovascular complications, including coronary artery disease, ischemia, rheumatic disease, rheumatoid arthritis, plaque disruption, thrombosis and atherosclerosis. The mastery of the inflammatory responses necessitates the development of new approaches to the prevention and treatment of chronic diseases associated with aging, such as atherosclerosis (Libby, 2007).

Although inflammation was previously considered as being a response to development of atheromatous vascular damage, it is now considered as the main causing factor in atherosclerosis rather than being its result. In this regard, a dramatically increased risk of cardiovascular disease has been reported in patients with pre-existing inflammatory diseases. Also, patients with autoimmune disorders including lupus erythematous and rheumatoid arthritis have higher rates of cardiovascular diseases such as atherosclerosis (Franceschi et al. 2000). Untreated infections such as periodontal disease which cause inflammation are associated with increased risk of cardiovascular complications (Candore et al. 2010).

The inflammation mediators have been shown to participate in atheromatous changes and vascular insults. Secretion of a host of inflammatory factors might contribute to the increased cardiovascular risks. The cardio-protective effects of many of drugs are mediated through improvement of systemic inflammation. The targeted suppression of various pro-inflammatory cascades in adipocytes specifically represents an exciting new therapeutic opportunity for the cardiovascular disease area (Berg and Scherer 2005).

The mechanisms underlying cardiovascular complications by systemic inflammation are not established. Type 2 diabetes mellitus, hypercholesterolemia, atherosclerosis, hypercoagulability, and metabolic syndrome are associated with coronary vasculopathy, and with circulating serum factors which mediate the connections between these disease conditions. These circulating mediators are mostly participated in systemic inflammation. Therefore, these factors may show the evidence for their connections with cardiovascular pathology (Berg and Scherer 2005; Rafieian-Kopaei 2014).

Inflammaging and cardiovascular diseases

The association between systemic inflammation and increase in the risk of cardiovascular diseases has stimulated basic and clinical investigators to research for precise nature and the differences in the nature of traditional inflammation and inflammaging in relation to cardiovascular diseases. In this regard, although their different roles in accelerating atherogenesis remain unresolved, however, it is known that inflammatory response in elderly is not as fast as younger individuals. Inflammation can be beneficial facilitating the adaptation, turnover and repair of many tissues. However, this inflammatory response might be impaired during aging which increase the susceptibility to pathogens (Griendling and FitzGerald 2003).

More importantly, in aging period, a host of molecular and cellular changes including genetic, epigenetic and environmental events occur which increase the progression of arterial diseases.

In aged people, the tissues are mostly in a chronically inflamed state, with no sign of infection. The generation of free radicals also increases, and makes aged people susceptible to cardiovascular diseases (Asadbeigi et al. 2014).

Inflammaging is associated with increased levels of IL-1, IL-6, TNF and CRP which are independent risk factors for mortality and morbidity. In aging process interference occurs with anabolic signaling, IL-6 and tumor necrosis factor-a increase, down-regulating insulin and insulin-like growth factor-1, as well as erythropoietin signaling and protein synthesis. Inflammaging can be due to the accumulation of damaged macromolecules and cells which increases with age due to increased production and/or inadequate elimination. Inflammaging might also be due to increase in harmful agents produced by microorganisms of the human body, including gut microbiota. In aging period, the gut microbiota may change and the capability of the gut to sequester these microbes and their products declines, leading to chronic inflammation (Pawelec, 1999).

Increase in inflammation in aging also might be due to high level of cellular response to stress and damage (cellular senescence). Senescent cells likely fuel age-related diseases such as cardiovascular disease, because they secrete numerous proinflammatory cytokines, modifying the tissue microenvironment and altering the function of nearby normal cells. Immunosenescence also contributes to inflammaging. In aging the adaptive immunity decreases and the innate immunity increases resulting in mild hyperactivity, which may lead to local inflammatory reactions in elderly people. Coagulation is considered as a part of the inflammation system. Increase in activation of the coagulation system in age people also can increase the inflammation. The higher incidence of thrombosis in the elderly has been attributed to hypercoagulable state in elderly people (Beige et al. 2002).

Oxidative stress in cardiovascular complications

Reactive oxygen species induced oxidative stress play a crucial role in development of vasculopathies, such as hypertension, atherosclerosis and restenosis after angioplasty. Although atherosclerosis was initially suggested to be the result of an injury to endothelial cells and subsequent macrophage infiltration, however, LDL oxidation and its implication in formation of fatty streaks are very important in process of atherogenesis (Griendling and FitzGerald 2003).

Various free radicals are produced in cardiovascular system and play a crucial role in vascular physiology as well as pathophysiology; the most important of them are superoxide ([O.sub.2.sup.*-]), hydrogen peroxide ([H.sub.2][O.sub.2]), peroxynitrite (ONO[O.sup.*-]) and nitric oxide (N[O.sup.*]). In vasculature. superoxide reacts with nitric oxide to form the highly reactive molecule of peroxynitrite (ONO[O.sup.*-]) which has an important role in protein nitration and lipid peroxidation. One of the most important productions of lipid peroxidation is LDLox (Oxidized low density lipoprotein) which has crucial role in atherogenesis (Madihi 2013a,b).

Nitric oxide is produced normally by endothelial nitric oxide synthase (eNOS), but in process of inflammation, inducible NOS can also be expressed in smooth muscle cells and macrophages (Asgary et al. 2014).

Nitric oxide plays an important role in platelet aggregation. Nitric oxide which is an important mediator of endothelium-dependent vasodilation also has a crucial role in maintaining smooth muscle cell growth and function (Rafieian-Kopaei et al. 2014c).

The function of most of free radicals including superoxide and hydrogen peroxide on cardiovascular system is critically dependent on the amounts produced (Rafieian-Kopaei et al. 2013; Nasri and Rafieian-Kopaei 2014). In low concentrations, they modulate the function of biochemical pathways mediating the responses such as growth of vascular smooth muscle cells (Rafieian-Kopaei et al. 2013; Rafieian-Kopae et al. 2014d). However, in high concentrations, free radicals can cause DNA damage and apoptosis as demonstrated in smooth muscle and endothelial cells (Rafieian-Kopaei 2014; Baradaran et al. 2014). Pathological inflammation is generally associated with excess free radicals and in advanced age the generation of free radicals increases, especially in cardiovascular system. More importantly, chronic inflammation makes aged people susceptible to age-related diseases, including cardiovascular complications (Franceschi et al. 2000).

Prevention and treatment strategies

Anti-inflammatory drugs

When the inflammatory response is no longer needed, it should be terminated to prevent unnecessary bystander damage to tissues. The most important anti-inflammatory drugs include nonsteroidal anti-inflammatory drugs (NSAIDs), glucocorticoids, and disease-modifying agents of rheumatoid diseases (DMARDs) (Singh 2012). NSAIDs and glucocorticoids are used in order to relieve symptoms, while, DMARDs are used with the aim of reducing or preventing tissue damage which are caused by inflammatory attack. Unfortunately, all of these have unacceptable side effects. Moreover, it is necessary to find out drugs for very long period of times in order to design a successful anti-inflammatory therapy for chronic disease. However, more potent anti-inflammatory therapy, usually has greater chance for adverse effects to host defense. For example, increased risk for infections are more observed in patients taking anti-TNFa therapy (Tabas et al. 2013). Nowadays, more attention has been paid to medicinal plants with antioxidant activity.

Potential role of antioxidants

Although free radicals are able to damage cells or its components by oxidizing proteins or DNA or causing lipid peroxidation, but they also possess crucial useful physiological functions. The useful function of antioxidant systems should not be removal of free radicals entirely, but instead keeping oxidative stress at a level below which they would trigger the inflammatory cascade, a series of intra-nuclear and intra-cellular signaling which results in the release of destructive inflammatory cytokines (Valko et al. 2007).

Progress has been made regarding the role of the signaling cascades in inflammatory process and early studies have also suggested that antioxidants might be useful in the treatment of vascular diseases (Hall Ratclife 1949). Studies on the effects of vegetables and fruits with antioxidant activity, less or more, have suggested reduction in cardiovascular morbidity and mortality (Verlangieri et al. 1985), particularly in regard to ischemic heart disease (Gey and Puska 1989; Emmert and Kirchner 1999).

Some studies on combinations of antioxidant drugs and vitamins have also had positive results. Consumption of 800 IU/day vitamin E in patients with prevalent cardiovascular disease showed reduction in the myocardial infarction (Boaz et al. 2000).

In another study in India, combined consumption of vitamins A, C, E, and beta-carotene were protective against oxidative stress and cardiac necrosis. They also were useful in reduction of the cardiac events and in preventing complications (Singh et al. 1996).

Combined supplementation with vitamins C and E reduced the progression of carotid atherosclerosis (Salonen et al. 2000). Probucol alone or in combination with antioxidant vitamins seems to be effective in reduction of subsequent restenosis rates (Tardif et al. 1997; Yokoi et al. 1997).

Most of the above mentioned studies are modest in size and involved subgroups where more than one antioxidant (combinations therapy) was used. However, in large randomized clinical trials the results were not all consistent with results of the above mentioned studies. Pooled data from over 77,000 subjects and randomized trials of vitamin E as well as 6 trials of [beta]-carotene with over 131,000 participants revealed that the vitamin E was not effective and [beta]-carotene consumption was associated with a worse outcome (P = 0.003).

A large, long-term trial, on women at high risk for cardiovascular diseases reported that vitamin C, vitamin E or [beta] carotene had no significant effect on cardiovascular events (Cook et al. 2007). Another large trial in Cambridge on the effects of vitamin C or vitamin E also revealed no significant reduction on the risk of major cardiovascular events (Sesso et al. 2008). Although the statistical analyses have suggested overall significance of antioxidant therapy in some studies, only those trials using probucol with or without antioxidant vitamins showed significant effect (Tardif et al. 1997). N-Acetylcysteine, in a trial on acute coronary syndrome, also produced significant improvement in cardiac index in patients treated with streptokinase (Arstall et al. 1995).

Hence, there it is necessary to search for more scientific evidence of the relative contribution of antioxidant constituents in inhibition and progression of cardiovascular events (Badimon et al. 2010).

Anti-inflammatory plants

Targeting the desired pathway through treating inflammation is not easy because of a wide range of changes in pathology as a consequence of existence of many inflammatory mediators and pathways in inflammation (Qiuhong et al. 2013).

Cyclooxygenase and lipoxygenase pathways and possibly some other mechanisms of initiation of inflammation can be efficiently stopped by some of the phytochemicals found in certain plants as well as aspirin (Lavet et al. 2013). NSAIDs and corticosteroids have an extensive use in the current treatment of inflammatory disorders in Western medicine. Lately, phytochemicals and their anti-inflammatory efficacies have attracted more attention in treatment of inflammation. Therefore; we tried to list and introduce some of these kinds of herbal drugs in this study (Xu et al. 2007).

Symptoms of several inflammatory diseases can be inhibited by Chinese Material Medica, such as Qijie Granule including the root of Astragalus membranaceus, the resin of Dranaena cochinchinensis (Lour.) S.C. Chen, the root of Angelica sinensis (Oliv.), Diels, the dried twig of Cinnamomum cassia Presl (Zhang et al. 2004), the dried rattan of Sargentodoxa cuneata (Oliv.) Rehd. etwils, the root of Rheum palmatum L., the resin of Commiphora myrrha Engl., the root of Paeonia lactiflora Pall., and the root of Glycyrrhiza uralensis Fisch, which are proven to have acceptable curative effects in treating chronic pelvic inflammation through improving the blood viscosity and regulating T-lymphocytic sub groups (Zhao et al. 2010). Contrasting with western drugs; boiling, steaming, treating with salt or vinegar, frying, or charring as some specific treatments are subjecting before use of these plants in decoctions or in the manufacture of herbal products (Aggarwal and Shishodia 2006).

It has been shown that active ingredients from medicinal plants play a significant part in the prevention and treatment of inflammatory diseases (Schepetkin and Quinn 2006). A characteristic of medicinal plants is their unique structural diversity and wide-ranging of pharmacological effects in contrast with common synthetic anti-inflammatory drugs (Qiuhong et al. 2013).

Recently, polysaccharides, which are widely used in the biomedical field as a result of their therapeutic effects and relatively low toxicity (He et al. 2012), are screened for their anti-inflammatory activities based on their unique structures in herbal plants. For example, it has been revealed that the main component of Astragalus membranaceus Bunge and Astragalus polysaccharides, have anti-inflammatory ability involving the inhibition of TNF-[alpha] and IL-1[beta] and reduction of nuclear factor-kb (NF-k[beta]) activity (Quang et al. 2012). The challenging part of using the polysaccharide drugs is the difficulty of targeting a specific location not only because of their large molecular weight but also due to their easy digestion and oral degradation by oral delivery. Hence, it seems that it is essential to set up the smallest effective parts of the structure and a useful form of direction for anti-inflammatory polysaccharides in further studies (Mendes et al. 2012).

It has been reported that essential oils of some medicinal plants have significant anti-inflammatory activities (Dunga et al. 2009). For example, secretion of pro-inflammatory cytokines such as TNF-[alpha], IL-1[beta], and NF-[kappa][beta] in RAW264.7 cells, a mouse macrophage-like cell line, that are induced by lipopolysaccharide (LPS) can be obviously prevented by applying the essential oil of the buds of Cleistocalyx operculatus (Roxb.) Merret Perry. Additionally, this oil can suppress the nuclear translocation of the p65 subunit and has the ability of inhibiting a phorbolester-induced which caused ear swelling and the water content of the skin in BALB/c mice (Lin et al. 1997). All together, these results suggest the anti-inflammatory effect of these essential oil extracts by suppressing the expression of pro-inflammatory cytokines.

It is proven that alkaloids are the main bioactive components in anti-inflammatory treatments, such as matrine. Matrine is extracted from the root of Sophora flavescens Ait, in order to use in treatment of some inflammatory diseases, such as enteritis, hepatitis and atopic dermatitis by inhibiting the activation of inflammatory signal and also, expression of pro-inflammatory mediators in human skin keratinocytes, fibroblasts, Kupffer cells, and rat intestinal microvascular endothelial cells (Liu et al. 2007; Zhang et al. 2008; Cheng et al. 2009; Zhang et al. 2011). Moreover, it has been found that the alkaloid, matrine, can reduce the increased levels of TNF-[alpha], IL-6 and HMG[beta]1 induced by LPS, in both in vivo and in vitro situations (Havsteen 1983) (see the table).

Citrus fruits, tea and wine are good sources for a wide range of bioflavonoids, with the ability of reducing inflammation by inhibiting cyclooxygenase and lipoxygenase pathways (Heim et al. 2002). Flavonoids, are one of the important members in anti-inflammatory components category, with a large family of compounds which represent varied biological properties and having the ability of suppressing the expression of inflammatory proteins and cytokines (Hu and Kitts 2003; Kim et al. 2004). Flavanoieds have been used in the form of crude plant extracts for their anti-inflammatory effects. For example, it has been confirmed that flavonoids are the major bioactive flavones in Radix Scutellariae (the root of Scutellariae baicalensis Georgi.), existing in the forms of aglycones (baicalein, wogonin, oroxylin A) and glycosides, which are used for the treatment of inflammatory diseases.

Luteolin, 3',4'-dihydroxyflavone, galangin, morin and apigenin as some examples of flavonoieds are proven to be inhibitors of COX, whereas some flavones/ flavonols/isoflavones, mainly flavones, significantly inhibit production of NO, as well (Abad-Martinez et al. 2005). Some of these compounds have been previously isolated and identified in B. incarum, B. boliviensis and P. lucida (Zampini et al. 2008; Calle et al. 2012; D'Almeida et al. 2013). D'Almeida et al. demonstrated that P. lucida extract inhibits arachidonic acid metabolism via several enzymes (COX, LOX and phospholipase A2).

Steroidal saponins are naturally found in the roots and barks of various Chinese herbs, which possess anti-inflammatory effects, such as: anemar saponin B, a steroidal saponin which are isolated from the rhizomes of Anemarrhena asphodeloides Bge by decreasing the protein and mRNA levels of iNOS and COX-2. Similar to flavonoids, steroidal saponins decrease the expression and production of proinflammatory cytokines, as well as TNF-[alpha] and IL-6. Additionally, the p65 subunit of NF-kB is obviously inhibited by phosphorylation of inhibitory kappa [beta]-a (Qiuhong et al. 2013).

Phenyl-propanoids are important components of the anti-inflammatory plants. Honokiol, as a member of phenyl propanoid component can be isolated from the herb Magnolia officinalis Rehd. etwils. (Qiuhong et al. 2013). It seems that saponins act as therapeutic agents on atherosclerosis by their anti-inflammatory activity, involving NF-k[beta] signaling pathway (Qiuhong et al. 2013). Table 1 shows the anti-inflammatory compounds of plant origin with their mechanisms actions.

Conclusion

Inflammation is an acute or chronic process and a defense response to injury, autoimmune response, tissue ischemia or infectious agents. Acute inflammation is a primary defense against injury or infection and a suitable stimulus factor in the healing process. It is usually beneficial, starts quickly, and then becomes severe. Chronic inflammation, occurring after acute inflammation, is not favorable to the system. Chronic inflammation has significant role in most of the chronic disease such as diabetes mellitus, atherosclerosis, Crohn's disease, cancer, ulcerative colitis and CNS disorders, which have briefly discussed in the present study.

Obviously, chronic diseases involve very suffering ones, so that it has been tried to find drugs with low side effects in order to design a successful anti-inflammatory therapy for. Medical plants can be applied because of their structural diversity and wide-ranging of pharmacological effects in contrast with common synthetic anti-inflammatory drugs. One of the good strategies that can be sufficiently used is extracting or isolating components from medical plants in order to develop anti-inflammatory drugs. It should be note that the pathological inflammation is associated with production of excess free radicals and medicinal plants mostly counteract oxidative stress by reducing free radicals (Asadi-Samani et al. 2014; Bahmani et al. 2014). Therefore, isolation of anti-inflammatory compounds may not be associated with antioxidant activity.

At the present study, we tried to not only explain inflammation, disease and its treatments with concentration on medical plants but collected a sufficient collection of anti-inflammatory plants with focusing on their mechanism of action. But as far as the huge number of existent herbs around the world collecting all together seems to be impossible.

ARTICLE INFO

Article history:

Received 23 August 2015

Revised 6 November 2015

Accepted 10 November 2015

Conflict of interest

The authors declare that there is not any conflict of interest.

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Erfaneh Shayganni (a), Mahmoud Bahmani (b), Sedigheh Asgary (c), Mahmoud Rafieian-Kopaei (a),*

(a) Medical Plants Research Center, Shahrekord University of Medical Sciences, Shahrekord, Iran

(b) Food and Beverages Safety Research Center, Urmia University of Medical Sciences, Urmia, Iran

(c) Isfahan Cardiovascular Research Center, Isfahan University of Medical Sciences, Isfahan, Iran

Abbreviations: CVD, Cardiovascular diseases; NOS, Nitric oxide synthase; eNOS, Endothelial nitric oxide synthase; LDLox, Oxidized low density lipoprotein; NSAIDs, Nonsteroidal anti-inflammatory drugs; DMARDs, Disease-modifying agents of rheumatoid diseases; NF-k[beta], Nuclear factor-kb.

* Corresponding author. Tel./fax: +98 383 3330709.

E-mail address: rafieian@yahoo.com (M. Rafieian-Kopaei).

http://dx.doi.org/10.1016/j.phymed.2015.11.004
Table 1
Anti-inflammatory compounds of plant origin.

Compounds                             Uses

Seeds of Phaseolus angularis Wight    Anti-inflammation

Bark of Cinnamomum cassia Blume       "

Dried roots Asparagus                 "
  cochinchinensis Merrill

Aerial of Houttuynia cordata Thunb    "

Roots of Scutellaria                  "
  baicalensis Georgi

Aerial part of Andrographis           "
  paniculata

The fruits of Forsythia               "
  koreana Nakai

Dried heart wood of                   "
  Caesalpinia sappan L.

Corolla of Carthamus                  "
  tinctorius L

Inflorescence of Chrysanthemum        "
  indicum Linne

Ripe fruit of Evodia                  "
  rutaecarpa

Roots of Clycyrrhiza uralensis        "
  Fisch.

Roots of Polygala tenuifolia          "
  Willd.

Dried bark of Phellodendron           "
  chinense Schneid.

Fruit of Vitex trifolia L.            "

Pericarp of Zanthoxylum               "
  schinifolium Sieb. et Zucc

Roots of Angelica sinensis (Oliv.)    "
  Diels

Roots of Clematis chinensis           "
  Osbeck

Leaves of Piectranthus                "
  amboinicus (Lour.) Spreng

Branches and leaves of Taxillus       "
  liquidambaricola Hosokawa

Aerial part of Pogostemon cablin      "
  (Blanco) Be nth

Young shoot of Aralia elata           "
  Seemann

Flower of Clossogyne tenuifolia       "
  Cass

Dried roots of Alpinia conchigera     "
  Griff

Roots of Sophora alopecuroides L.     "

Leaves of Cisfus Lourifolius Linn.    Inflammatory ailments such
  (Cistaceae)                           as rheumatism and renal
                                        inflammation

Roots of Daphne pontica Linn.         Anti-tumor
  (Thymelaeceae)

Fruit rinds of Garcinia               Treatment of trauma and
  mangostana Linn. (Guttiferas;         skin infections
  Clusiaceae)

Fruit of Gardenia jasminoides         Treatment of inflammation
  Ellis (Rubiaceae)

Leaves of Piper ovatum Vahl           Treatment of inflammation
  (Piperaceae)

Hydroethanolic (70%) extract          "
  of Macrosiphonia longiflora

B. incarum, Baccharis                 "
  boliviensis, Ch. atacamensis
  and P. lucida ethanolic
  extracts

J. seriphioides and P.                "
  lepidophylla extracts

Essential oil of Eugenia              Nasal obstruction,
  caryophyllata                         musculoskeletal pain,
                                        inflammation

on COX-2 activity                     (Ozturk and Ozbek 2005)

Ethanol extracted of Desmodium        Injuries
  pauciflorum, Mangifera indica
  and Andrographis paniculata

Curcumin (a naturaliy-occuring        Atherosclerosis, Alzheimer's
  yellow pigment present in the         disease, Arthrits and
  rhizomes of the plant curcuma         Pancreases
  Longa L (Zingiberaceae))

Resveratol (phytoalexin               Anticarcinogenic and
  polyphenol) present in grape          anti-platelet activity
  skin, red wines and other
  plants

Flavonoids baicalein (isolated        Anticancer agent
  from roots of scutellaria
  baicalensis Georgi (Lamiaceae)

Cirsilio (isolated from               Leuchemia
  achillea fragrantissima Forssk
  (Asteraceae)), Luteolin, morin

Chrysin, apigenin and                 Anti-inflammatory activity
  pheloretin

Silbin, silydian and                  Anti-inflammatory activity
  silychristin, (from silybum
  marianum L (Milk thistle)
  (Asteraceae)

Biflavon (from ginkgo biloba L        Arthtitic inflammation
  (ginkgoaceae)

Tectorigenin and tectoridin           Anti-inflammatory activity
  (isolated from rhizomes of
  belomcanda chinensis L.
  (Iridaceae))

Platycodin D (isolated from           "
  roots of platycodon
  grandiflorum A.
  (campanulaceae)

Ursolic acid and oleanic acid         "
  isomers (extracted from
  plantago major L.
  (plantaginaceae)

B-tumerone and artumeron              Respiratory problems
  (sesquiterpens from Curcuma
  zedoaria L. (Zingiberaceae)

Fatty acids extracted from            Anti-inflammatory activity
  Plantago major L.
  (Plantaginaceae)

CAPE (Caffeic acid phenetyl           Anti-inflammatory,
  ester, a cpumpond produced by         anticarcinogenic,
  honeybees from the gum of             anti-mitogenic and
  various plants)                       immunomedulator

Quinazolinocarboline alkaloid         Antithrombotic effect
  rutacarpine (from Evodia
  rutaecarpa Bentham (Rutaceae))

Aqueous and alcholic extract          Treatment of gastro-intestinal
  of Achillea millefolium Linn.         and hepato-biliary
  (Asteraceae)                          disorders, skin
                                        inflammasion

Aspilia africina (Pars.)              Stops blood flow from
  (Asteraceae)                          fresh wounds, traditional
                                        treatment of malaria

Ethanolic extract of Bacopa           Treatment of bronchitis,
  monnieri (Linn.) penn                 asthma and rhumatism
  (scrophulariacceae)

Chloroform extract of                 Anti-inflammatory activity
  Bryonopsis Laciniosa (Linn.)          in chronic and acute
  (Cucurbitaceae)                       disease

Neptin (isolated from                 Hepatoprotective and
  dichloromethane extract of            against fever and
  arial parts of Eupatorium             rheumatism
  amottianum Grieseb.
  (Asteraceae)

Compounds                             Mechanism of action

Seeds of Phaseolus angularis Wight    Dercreases NO, PGE2, iNOS,
                                        COX2, NF-[kappa][beta]

Bark of Cinnamomum cassia Blume       Decreases NO iNOS, COX2,
                                        NF-[kappa][beta]

Dried roots Asparagus                 Decreases MPO
  cochinchinensis Merrill

Aerial of Houttuynia cordata Thunb    Decreases NO, COX2

Roots of Scutellaria                  Decreases IL2, IL6, IL12,
  baicalensis Georgi                    IL1[beta], TNF-[alpha],
                                        NF-[kappa][beta],
                                        I[kappa][beta]

Aerial part of Andrographis           Decreases IL6, COX2,
  paniculata                            IL1[beta], TNF-[alpha]

The fruits of Forsythia               Decreases NO, iNOS, COX-2
  koreana Nakai

Dried heart wood of                   Decreases NO, PGE2, iNOS,
  Caesalpinia sappan L.                 COX2, Il-6, IL1[beta],
                                        TNF-[alpha], and increases
                                        IL10

Corolla of Carthamus                  Decreases NO, PGE2, iNOS,
  tinctorius L                          COX2, NO, iNOS TNF-[alpha],
                                        NF-[kappa][beta]

Inflorescence of Chrysanthemum        Decreases NO, PGE2, iNOS,
  indicum Linne                         COX2

Ripe fruit of Evodia                  Decreases NO, iNOS
  rutaecarpa

Roots of Clycyrrhiza uralensis        Decreases NO, iNOS, IL-6, NO,
  Fisch.                                NF-[kappa][beta],
                                        IL1[beta], 1[kappa][beta]

Roots of Polygala tenuifolia          Decreases NO, PGE2, iNOS,
  Willd.                                COX2, IL1[beta], TNF-[alpha]

Dried bark of Phellodendron           Decreases COX-2, IL-6
  chinense Schneid.

Fruit of Vitex trifolia L.            Decreases iNOS, IL-6,
                                        IL-1[beta], TNF-[alpha] and
                                        increases IL-10

Pericarp of Zanthoxylum               Decreases IL-8, TNF-[alpha],
  schinifolium Sieb. et Zucc            NF-[kappa][beta] ,
                                        I[kappa][beta]

Roots of Angelica sinensis (Oliv.)    Decreases iNOS, COX-2,
  Diels                                 IL1[beta], TNF-[alpha]

Roots of Clematis chinensis           Decreases COX-2, IL1[beta],
  Osbeck                                TNF-[alpha],
                                        NF-[kappa][beta]

Leaves of Piectranthus                Decreases COX-2, TNF-[alpha],
  amboinicus (Lour.) Spreng             NF-[kappa][beta],
                                        I[kappa][beta]

Branches and leaves of Taxillus       Decreases NO, iNOS, COX-2,
  liquidambaricola Hosokawa             TNF-[alpha]

Aerial part of Pogostemon cablin      Decreases, IL1[beta],
  (Blanco) Be nth                       TNF[alpha], NO, PGE2, iNOS,
                                        COX2, NF-[kappa][beta]

Young shoot of Aralia elata           Decreases IL1[beta],
  Seemann                               TNF[alpha], NO, PGE2,
                                        NF-[kappa][beta],
                                        I[kappa][beta]

Flower of Clossogyne tenuifolia       Decreases PGE2, iNOS, COX-2,
  Cass                                  IL-6, IL-12, IL1[beta],
                                        TNF-[alpha],
                                        NF-[kappa][beta]

Dried roots of Alpinia conchigera     Decreases NO, iNOS, IL1[beta],
  Griff                                 TNF-[alpha],
                                        NF-[kappa][beta]

Roots of Sophora alopecuroides L.     Decreases IL-6, IL1[beta]

Leaves of Cisfus Lourifolius Linn.    Inhibits activity of
  (Cistaceae)                           IL-l[alpha] and PGs

Roots of Daphne pontica Linn.         Inhibits production of PGE2
  (Thymelaeceae)                        and IL-1[beta]

Fruit rinds of Garcinia               Block production of iNOS and
  mangostana Linn. (Guttiferas;         COX-2
  Clusiaceae)

Fruit of Gardenia jasminoides         Block production of COX-2,
  Ellis (Rubiaceae)                     NF-[kappa][beta] and
                                        I[kappa][beta]

Leaves of Piper ovatum Vahl           Inhibitory effecr on
  (Piperaceae)                          production of COX-1

Hydroethanolic (70%) extract          Decreases IL-1[beta], IL-10
  of Macrosiphonia longiflora           and NO release, and
                                        possibly the PGs.

B. incarum, Baccharis                 Inhibit COX-1 and COX-2
  boliviensis, Ch. atacamensis          activities
  and P. lucida ethanolic
  extracts

J. seriphioides and P.                Effect on COX-2 activity
  lepidophylla extracts                 but not on the enzyme
                                        expression,

Essential oil of Eugenia              Inhibitory effect
  caryophyllata

on COX-2 activity

Ethanol extracted of Desmodium        Inhibition of prostoglandin
  pauciflorum, Mangifera indica         synthesis
  and Andrographis paniculata

Curcumin (a naturaliy-occuring        Inhibition of lipooxigenase
  yellow pigment present in the         and COX-2
  rhizomes of the plant curcuma
  Longa L (Zingiberaceae))

Resveratol (phytoalexin               Inhibition of COX-1 and COX-2
  polyphenol) present in grape
  skin, red wines and other
  plants

Flavonoids baicalein (isolated        Inhibition of 5-LO and LTC4
  from roots of scutellaria             and PGE2
  baicalensis Georgi (Lamiaceae)

Cirsilio (isolated from               Inhibits production of COX-2
  achillea fragrantissima Forssk        activity
  (Asteraceae)), Luteolin, morin

Chrysin, apigenin and                 inhibits COX-2 expression
  pheloretin                            and platelet aggregation

Silbin, silydian and                  Inhibit both LO and COX
  silychristin, (from silybum           activity
  marianum L (Milk thistle)
  (Asteraceae)

Biflavon (from ginkgo biloba L        Inhibit PLA2
  (ginkgoaceae)

Tectorigenin and tectoridin           Inhibits production of COX-2
  (isolated from rhizomes of
  belomcanda chinensis L.
  (Iridaceae))

Platycodin D (isolated from           Inhibits production of COX-2
  roots of platycodon
  grandiflorum A.
  (campanulaceae)

Ursolic acid and oleanic acid         inhibit production of COX-2
  isomers (extracted from
  plantago major L.
  (plantaginaceae)

B-tumerone and artumeron              Inhibit LPS-induced PGE2
  (sesquiterpens from Curcuma           production
  zedoaria L. (Zingiberaceae)

Fatty acids extracted from            Inhibit both COX-A and COX-2
  Plantago major L.
  (Plantaginaceae)

CAPE (Caffeic acid phenetyl           Inhibits both COX-A and COX-2
  ester, a cpumpond produced by
  honeybees from the gum of
  various plants)

Quinazolinocarboline alkaloid         Inhibit LPS-induced PGE2
  rutacarpine (from Evodia              production, inhibition of
  rutaecarpa Bentham (Rutaceae))        TXA2

Aqueous and alcholic extract          Inhibition of arachidonic
  of Achillea millefolium Linn.         acid
  (Asteraceae)

Aspilia africina (Pars.)              Inhibit action of mediators
  (Asteraceae)                          like histamine, 5-HT,
                                        kinins and prostanoieds

Ethanolic extract of Bacopa           Suppres PGE1, bradykinin
  monnieri (Linn.) penn                 and serotonin
  (scrophulariacceae)

Chloroform extract of                 Inhibits increasing of
  Bryonopsis Laciniosa (Linn.)          fibroblasts and synthesis
  (Cucurbitaceae)                       of mucopolysacharids during
                                        formation of granuloma

Neptin (isolated from                 Inhibits NF-[kappa][beta]
  dichloromethane extract of            activity
  arial parts of Eupatorium
  amottianum Grieseb.
  (Asteraceae)

Compounds                             reference

Seeds of Phaseolus angularis Wight    (Yuet al. 2011)

Bark of Cinnamomum cassia Blume       (Yu et al. 2012)

Dried roots Asparagus                 (Lee et al. 2009)
  cochinchinensis Merrill

Aerial of Houttuynia cordata Thunb    (Li et al. 2011c)

Roots of Scutellaria                  (Kimet al. 2009a)
  baicalensis Georgi

Aerial part of Andrographis           (Parichatikanond et al. 2010)
  paniculata

The fruits of Forsythia               (Lim et al. 2008)
  koreana Nakai

Dried heart wood of                   (Wang et al. 2011)
  Caesalpinia sappan L.

Corolla of Carthamus                  (Junet al. 2011)
  tinctorius L

Inflorescence of Chrysanthemum        (Wu et al. 2011c)
  indicum Linne

Ripe fruit of Evodia                  (Ko et al. 2007)
  rutaecarpa

Roots of Clycyrrhiza uralensis        (Yu et al. 2012)
  Fisch.

Roots of Polygala tenuifolia          (Cheng et al. 2005)
  Willd.

Dried bark of Phellodendron           (Xian et al. 2011)
  chinense Schneid.

Fruit of Vitex trifolia L.            (Matsui et al. 2009)

Pericarp of Zanthoxylum               (Cheonget al. 2011)
  schinifolium Sieb. et Zucc

Roots of Angelica sinensis (Oliv.)    (Cao et al. 2009)
  Diels

Roots of Clematis chinensis           (Peng et al. 2011)
  Osbeck

Leaves of Piectranthus                (Deng et al. 2011)
  amboinicus (Lour.) Spreng

Branches and leaves of Taxillus       (Deng et al. 2011)
  liquidambaricola Hosokawa

Aerial part of Pogostemon cablin      (Li et al. 2011)
  (Blanco) Be nth

Young shoot of Aralia elata           (Suhet al. 2007)
  Seemann

Flower of Clossogyne tenuifolia       (Wu et al. 2004)
  Cass

Dried roots of Alpinia conchigera     (Lee et al. 2006)
  Griff

Roots of Sophora alopecuroides L.     (Wang et al. 2012c)

Leaves of Cisfus Lourifolius Linn.    (Kupeli and Yesilada 2007)
  (Cistaceae)

Roots of Daphne pontica Linn.         (Kupeli and Yesilada 2007)
  (Thymelaeceae)

Fruit rinds of Garcinia               (Chen et al. 2008)
  mangostana Linn. (Guttiferas;
  Clusiaceae)

Fruit of Gardenia jasminoides         (Koo et al. 2006)
  Ellis (Rubiaceae)

Leaves of Piper ovatum Vahl           (Siva et al. 2008)
  (Piperaceae)

Hydroethanolic (70%) extract          (Alberto et al. 2009)
  of Macrosiphonia longiflora

B. incarum, Baccharis                 (Calle et al. 2012)
  boliviensis, Ch. atacamensis
  and P. lucida ethanolic
  extracts

J. seriphioides and P.                (Torres Carro et al. 2007)
  lepidophylla extracts

Essential oil of Eugenia
  caryophyllata

on COX-2 activity

Ethanol extracted of Desmodium        (Shirani et al. 2011)
  pauciflorum, Mangifera indica
  and Andrographis paniculata

Curcumin (a naturaliy-occuring        (Song et al. 2001)
  yellow pigment present in the
  rhizomes of the plant curcuma
  Longa L (Zingiberaceae))

Resveratol (phytoalexin               (Jangand Pezzutto 1999)
  polyphenol) present in grape
  skin, red wines and other
  plants

Flavonoids baicalein (isolated        (Middelton et al. 2000)
  from roots of scutellaria
  baicalensis Georgi (Lamiaceae)

Cirsilio (isolated from               (Lindolfi et al. 1984)
  achillea fragrantissima Forssk
  (Asteraceae)), Luteolin, morin

Chrysin, apigenin and                 (Rasoet al. 2001)
  pheloretin

Silbin, silydian and                  (Gupta et al. 2000)
  silychristin, (from silybum
  marianum L (Milk thistle)
  (Asteraceae)

Biflavon (from ginkgo biloba L        (Kimet al. 1999)
  (ginkgoaceae)

Tectorigenin and tectoridin           (Yamki et al. 2002)
  (isolated from rhizomes of
  belomcanda chinensis L.
  (Iridaceae))

Platycodin D (isolated from           (Kim et al. 2001)
  roots of platycodon
  grandiflorum A.
  (campanulaceae)

Ursolic acid and oleanic acid         (Suhet al. 1998)
  isomers (extracted from
  plantago major L.
  (plantaginaceae)

B-tumerone and artumeron              (Hong et al. 2002)
  (sesquiterpens from Curcuma
  zedoaria L. (Zingiberaceae)

Fatty acids extracted from            (Ringbom et al. 2001)
  Plantago major L.
  (Plantaginaceae)

CAPE (Caffeic acid phenetyl           (Michaluat et al. 1999)
  ester, a cpumpond produced by
  honeybees from the gum of
  various plants)

Quinazolinocarboline alkaloid         (Woo et al. 2001)
  rutacarpine (from Evodia
  rutaecarpa Bentham (Rutaceae))

Aqueous and alcholic extract          (Benedik et al. 2007)
  of Achillea millefolium Linn.
  (Asteraceae)

Aspilia africina (Pars.)              (Okoli et al. 2007)
  (Asteraceae)

Ethanolic extract of Bacopa           (Channa et al. 2006)
  monnieri (Linn.) penn
  (scrophulariacceae)

Chloroform extract of                 (Gupta et al. 2003)
  Bryonopsis Laciniosa (Linn.)
  (Cucurbitaceae)

Neptin (isolated from                 (Okoli et al. 2007)
  dichloromethane extract of
  arial parts of Eupatorium
  amottianum Grieseb.
  (Asteraceae)
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Author:Shayganni, Erfaneh; Bahmani, Mahmoud; Asgary, Sedigheh; Rafieian-Kopaei, Mahmoud
Publication:Phytomedicine: International Journal of Phytotherapy & Phytopharmacology
Article Type:Report
Date:Sep 28, 2016
Words:8685
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