Printer Friendly

Anti-inflammatory and antioxidant activity of Strychnos nux vomica Linn.

Introduction

It is now well established that free radicals have been implicated in a vast number of diseases, ranging from cancer, through autoimmune conditions, to acute and chronic inflammatory disease including rheumato id arthritis (Halliwell, 1987, Halliwell and Gutteridge 1999; Winrow, et al., 1993; Mahajan and Tandon, 2004). This has led to increased interest amongst the researchers globally to evaluate role of antioxidant therapy in inflammatory diseases. In spite of the discovery of several newer agents, the search for better anti-inflammatory drugs continues because they have many known side effects and none of them is suitable for prolonged use. The side effects of the anti-inflammatory drugs are one of the major problems in developing medicine today. Therefore, development of new and more powerful drugs with fewer side effects is needed.

Natural products have long been recognized as an important source of therapeutically effective medicines. Large numbers of herbal drugs are in use for the treatment of arthritis by Ayurvedic and Siddha practitioners. Ayurveda recommends the use of Stychnos nux vomica Linn. in purified form since time immemorial in treatment of various diseases. Seeds are bitter, insecticidal, aphrodisiac, appetizer, tonic, antihelmintic, febrifuge, emmenagogue, purgative, stimulant and stomachic (Warrier et al., 1996). They are useful in anaemia, asthma, bronchitis, constipation, diabetes, insomnia, cardiopalmus, skin diseases, paralysis and weakness of limbs. Seeds are also used for nervous disorders (Jain & De Filipps, 1991). It is very effective in chicken pox fever. It is a tribal remedy for snake bite (Murthy et al, 1986). It is widely used in treatment of eczema (Maslmani et al., 1979 and 1981) and rheumatism (Choudhury, 1977; Sen et al, 1983; Shukla et al., 1985). Different formulations of this plant product are on the market, for treatment of rheumatoid arthritis and other metabolic ailments (Thakur et al., 1989; Chaurasia et al., 1995).

Antilipid pero xidative property of Strychnos nux vomica alcohol extract has been reported on cumene hydroperoxide (Tripathi and Chaurasia, 1996a) and ferrous sulphate (Tripathi and Chaurasia, 1996b) induced models of lipid peroxidation. It also possesses significant metal chelation property and chelated both forms of iron (Fe2+ and Fe3 +). Due to lack of redox behavoiur it does not act as prooxidant with transition metal ions (Tripathi and Chauras ia, 2000).

The present study was undertaken to screen the relationship between anti-inflammatory and antioxidant activity of S. nux vomica seed extract. The anti-inflammatory activity of Strychnos nux vomica Linn. extract was studied on acute and chronic phases of inflammation using carrageenan induced paw edema (Winter et al., 1962) and the cotton pellet granuloma test (Bailey, 1988), respectively. The efforts has been made to explain the mechanism of action by studying antioxidant property on enzymatic and non enzymatic models of lipid peroxidation induced by [Fe.sup.3+]-ADP (1.6 mM-62 [micro]M) and FeS[O.sub.4](0.5mM) respectively accompanied by measuring reduced glutathione level under normal and toxic condition. In order to evaluate antihepatotoxic activity of S. nux vomica extract, level of serum transaminases (SGOT and SGPT) was measured.

Materials and methods

Chemicals

Thiobarbituric acid (TBA), trichloro acetic acid (TCA), ferric chloride, ferrous sulphate and acetic acid were purchased from Central Drug House Pvt. Ltd. 1,1,3,3-tetra ethoxy propane(TEP), reduced glutathione (GSH), Adenosine di phosphate (ADP), 5,5-dithio-bis(2-nitro benzoic acid)(DTNB) and carrageenan were of Sigma Chemical Co., Louis, Mo. USA. All other chemicals were of analytical grade.

Plant Material

S. nux vomica seeds were purchased from the Ayurvedic Pharmacy, Institute of Medical Sciences, Banaras Hindu University. Their authenticity was verified on pharmacognostic parameters and with the direct comparison with the sample preserved in the department of Dravyaguna, IMS, BHU (Voucher No. 180). For its purification, an indigenous method, as described in Ayurvedic text (Bhanu and Vasudevan, 1986) was used as described earlier (Tripathi and Chaurasia, 1996a).

Preparation of alcohol extract

Dried purified seeds were powdered and exhaustively extracted with ethanol using soxhlet extractor for 48 hours. The resulting extract was distilled under reduced pressure in a Buchi type rotary evaporator. Concentrated extract (residue) was transferred to a vacuum desiccator and dried until constant weight was attained. The yield of solvent free extract was 32.9% (w/v). The extract was characterized by HPLC-fingerprint (Tripathi and Chaurasia., 1996b). This extract was suspended in a drug vehicle (Tween 80: water; 1:9) for a known concentration (w/v) and was stored at 40C until further use.

Animals

Inbred Albino rats of Charles Foster strain (100-150 g) of either sex were used for the pharmacological activities. They were kept in polypropylene cages at 25 [+ or -] 2[degrees] C, with relative humidity 45-55% under 12h light and dark cycles. All the animals were acclimatized to the laboratory conditions for a week before use. They were fed with standard animal feed (Hindustan Lever, Mumbai, India.) and water ad libitum. The animals were not fed for 12 hours before experiment.

Carrageenan induced paw oedema @@ The rats were divided into 5 groups (n = 6). Group I served as control, which received drug vehicle 10 [mlkg.sup.-1] b.w, p.o. (tween 80:water; 1:9), group II-V were pre treated with S. nux vomica extract (50, 100,150 and 200 [mgkg.sup.-1] b.w, p.o.) as per protocol. Paw oedema was induced by injecting 0.1ml of (1%, w/v) carrageenan in physiological saline into the subplantar tissues of the left hind paw of each rat (Winter et al., 1962). Animals were pretreated with different doses of drug for 7,15 and 30 days prior to Carrageenan administration. The paw volume was measured every hour till 3 h after carrageenan injection by the mercury displacement method using a plethysmograph. The percentage inhibition of paw volume in drug treated group was compared with the control group. The anti-inflammatory activity is expressed as the average percent inhibition of oedema in each group, which is calculated according to the general formula: % inhibition = (Vc - Vt)' 100/Vc, where Vt and Vc represent the average oedema volume of rats treated with drug and control, respectively.

Cotton pellet granuloma

The rats were divided into 5 groups (n = 18). Group I served as control, which received drug vehicle 10[mlkg.sup.-1] b.w, p.o. (tween 80:water; 1:9), group II-V were pre treated with S. nux vomica extract (50, 100, 150 and 200 [mgkg.sup.-1] b.w, p.o.) as per protocol. All five groups were sub divided into 3 subgroups (SG) (n=6). Subgroup 1 (SG1) was not pretreated with any drug. SG2 and SG3 were pretreated with different doses of drug for 7 and 21 days respectively. After completion of drug schedule, dry sterilized cotton pellets (10 [+ or -] 0.5 mg) were implanted subcutaneously into both sides of the groin region of each rat. Different drugs were continued for next 7 days. The pellets were taken out on 8th day, washed and dried at 60 C for 24 hr. The granuloma weight obtained from control and treated group s were us ed to calculate percentage inhibition (Bailey, 1988, Mukhopadhyay and Lahiri, 1992).

Activity of serum transaminases

Different doses (50-200 [mgkg.sup.-1] b.w, p. o.) o f S. nux vomica extract were given orally for 30 days. After completion of drug scohedule, blood was collected from brachial artery. Serum was separated and stored immediately at -20 C. Serum glutamic oxaloacetic transaminase (SGOT) and serum glutamic pyruvic transaminase (SGPT) were determined using commercial kit (J. Mitra & Co. Pvt. Ltd., New Delhi) based on the method of Reitman and Frankel (1957). Dinitro phenyl hydrazine used as substrate and absorbance was recorded at 520 nm against distilled water. Units of SGOT and SGPT were determined from the standard curve.

Preparation of rat liver homogenate

Rats were fixed on the operation table by ventral side up and dissected. Liver was perfused with normal saline through hepatic portal vein. Liver was harvested and its lobes were briefly dried between filter papers and were thin cut with a heavy-duty blade. These small pieces were then transferred to the glass Teflon homogenizing tube to prepare homogenate (10%, w/v) in Phosphate buffer saline (PBS) (pH 7.4) in cold condition. It was centrifuged at 3000 rpm for 10 minutes. The supernatant was finally suspended in PBS to contain approximately 0.8-1.5 mg protein in 0.1 ml of suspension, which was used to perform the in vitro experiment.

Lipid peroxidation assay (TBARS)

The degree of lipid peroxidation was as s ayed by estimating the thiobarbituric acid-reactive substances (TBARS) by using standard method (Ohkawa et al., 1979) with slight modifications (Pandey et al., 1994). 3 ml rat liver homogenate (5%) was taken in different 35 mm glass Petridishes. Different concentrations of plant extract and standard antioxidants (as per protocol) were p reinc ubated with homogenate for 10 min at 37[degrees]C. After incubation lipid peroxidation was induced enzymatically and nonenzymatically by adding [Fe.sup.3+]-ADP (1.6 mM-62 [micro]M) and FeS[O.sub.4] (0.5mM) respectively. Petridis hes were further incubated for 30 min. 100 [micro]l of incubation mixture (5% homogenate in PBS, pH 7.4) was transferred to a tube containing 1.5 ml 10% trichloro acetic acid. After 10 minutes, tubes were centrifuged at 5000 rpm for 10 minutes. Supernatant was mixed with 1.5 ml TBA (0.67% aqueous TBA in 50% acetic acid, 1:1). The mixture was kept in a boiling water bath for 30 minutes. Tubes were cooled and absorbance was taken at 535nm. The values were evaluated on the basis of a standard curve by using 1, 1, 3, 3-tetra ethoxy pro pane (TEP). Protein was estimated by the standard method (Lowry et al, 1951).

Reduced glutathione assay (GSH)

Reduced glutathione was determined by the method of Ellman (1959), 3 ml of 10% rat liver homogenate was taken in 35 mm Petridishes. In control only buffer was added, whereas in experimental groups all the agents such as extract, FeS[O.sub.4], vitamin E and parabenzoquinone (PBQ) were added in different combinations as per protocol. 250ml incubation mixture was mixed with 0.5 ml precipitating buffer (5% Trichloro acetic acid in 1mM ethylene diamine tetra acetic acid (EDTA). The sample was centrifuged at 2000 rpm for 10 min., and the supernatant mixed with 2.5 ml of 0.1 M phosphate buffer (pH 8.0). The colour was developed by adding 100 [micro]l 5,5-dithio bis (2-nitrobenzoic acid) (DTNB) (0.01%). Absorbance was determined at 412 nm. The concentration of reduced glutathione was evaluated by using the standard curve of reduced glutathione (GSH).

Statistical evaluation

Results given here are mean [+ or -] SD of six separate experiments. Level of significance has been calculated by using Student's t test

Results and discussion

Effect on carrageenan induced rat paw oedema

Interplantar injection of carrageenan in rats led to a time-dependent increase in paw thickness (Figure 1); this increase was observed at 1 h and was maximal at 3 h after administration. However, carrageenan-induced paw edema was significantly reduced in all phases of inflammation in a dose and duration dependent manner by treatment with S. nux vomica extract. Pretreatment with drug for 7 days, a maximum 40% inhibition in paw oedema formation was observed at a dose of 200 [mgkg.sup.-1] b.w, followed by 35%, 21% and 11% with 150, 100, 50 [mgkg.sup.-1] b.w respectively. On increasing the duration of drug treatment, the extent of oedema formation decreased significantly. At a dose of 200 [mgkg.sup.-1] b.w. for 7,15 and 30 days 40%,72% and 95% inhibition in oedema formation was found respectively. It shows that S. nux vomica is effective to check the inflammation on long term use.

[FIGURE 1 OMITTED]

Effect on cotton pellet granuloma

The effects of S. nux vomica extract on the proliferative phase of inflammation are shown in Table 1. A significant reduction in the weight of cotton pellets was observed with animals pretreated with extract for 7 and 21 days (SG2 and SG3) in comparison with control rats. Response was in a dose and time dependent manner. In Subgroup 1 (SG1) only 7% inhibition in granuloma formation was observed with a dos e of 50 [mgkg.sup.-1] which increased to 30% by increasing the dose of drug up to 200 [mgkg.sup.-1.] Antiinflammatory response also increased with increasing the duration of drug treatment. At a dose of 200 [mgkg.sup.-1] b.w inhibition in granuloma weight increased from 30% to 87%.

Effect on serum transaminases

Results (Table 2) clearly indicate that there was no significant change in SGOT and SGPT activities in comparison to control. Thus it could be inferred that S. nux vomica up to a dose of 200 [mgkg.sup.-1] body weight is totally safe when given to normal rats for a long duration of 30 days.

Protective effect of S. nux vomica on lipid peroxidation

Strychnos nux vomica extract showed significant reduction in lipid peroxidation induced by FeS[O.sub.4] and [Fe3.sup.+]-ADP complex in a dose dependent manner (Table 3). Under similar experimental conditions result was compared with well known antioxidants Vitamin E and Parabenzoquinone (PBQ). Vitamin E and PBQ in increasing concentration inhibited both the models of lipid peroxidation. [ED.sub.50] for all the tree agents are determined by using dose response curve (Table 4).

Effect of S. nux vomica on reduced glutathione

Glutatathione in reduced form (GSH) is an important endogenous antioxidant. The result in Figure 2 indicated that in rat liver homogenate GSH undergo aerial oxidation and there is a gradual decrease in GSH content which reached the basal level in 50 minutes (control group). In presence of FeS[O.sub.4] (3.0 mM) there was a sharp depletion in GSH content. S. nux vomica extract significantly reduced the rate of oxidation of GSH even in presence of FeS[O.sub.4]. Under similar conditions, vitamin E and parabenzoquinone failed to maintain the GSH content. Interestingly PBQ enhanced the rate of oxidation of GSH, whereas vitamin E neither prevented nor enhanced GSH oxidation (Figure 3).

[FIGURE 2 OMITTED]

[FIGURE 3 OMITTED]

Discussion

Strychnos nux vomica was evaluated for its anti-inflammatory activity in acute and chronic models. Significant anti-inflammatory activity was observed in both carrageenan induced paw oedema and cotton pellet granuloma models. The extract showed maximum inhibition of 95% in carrageenan induced paw oedema at the dose of 200 [mgkg.sup.-1] b.w. when animals were pretreated with drug for 30 days. Carrageenan induced oedema is commonly used as an experimental animal model for acute inflammation (Winter, 1962). The development of oedema in the paw of the rat after injection of carrageenan was described by Vinegar et al. (1969) as a biphasic event. The initial phase observed during the first hour is attributed to the release of histamine and serotonin, the second phase is due to the release of prostaglandin-like substances The result of the present study indicates that S. nux vomica extract showed significant suppressive activity in both phases. Based on this, it could be argued that the suppression of the first phase may be due to inhibition of the release of early mediators, such as histamine and serotonin, and the action in the second phase may be explained by blocking any step from arachidonic acid release to prostaglandin formation by catalysis of cyclo-oxygenase.

Chronic inflammation includes a proliferation of fibroblasts and the infiltration of neutrophils and exudation (Spector, 1969; Swingle and Shideman, 1972). These cells can be either spread or in granuloma form. Nonsteroidal anti-inflammatory drugs (NSAIDS) decrease the size of granuloma which results from cellular reaction by inhibiting granulocyte infiltration/inflammation, preventing generation of collagen fibers and suppressing mucopolysaccharides (Suleyman, 1999). The S. nux vomica extract showed significant antiinflammatory activity in cotton-pellet induced granuloma and thus found to be effective in chronic inflammatory conditions, which reflected its efficacy in inhibiting fibroblasts proliferation, synthesis of collagen and mucopolysaccharides during granuloma tissue formation. There was no rise in serum transaminases in all tested dose of S. nux vomica up to 30 days (Table 2). This finding supports its non-toxic effect at the therapeutic doses in rats.

Recent studies suggest that the inflammatory tissue damages are due to the liberation of reactive oxygen species from phagocytes invading the inflammation sites (Conner and Grisham, 1996; Winrow, 1993; Parke and Sapota, 1996). To investigate if the anti-inflammatory effect of S. nux vomica could be also related to antioxidant activity, the extract was evaluated on non enzymatic and enzymatic models of lipid peroxidation induced by FeS[O.sub.4] and [Fe3.sup.+]-ADP complex respectively in the rat liver ho mogenate (Bucher et al., 1983; Svingen et al., 1979; Hogeberg et al, 1975). The results (Table 3) clearly indicate the dose dependent protective response of S. nux vomica extract on both the models of lipid peroxiation (Table 3). Results were comparable to well known antioxidants (Table 4).

Glutathione is an important endogenous antioxidant, which plays an important role in protecting cells against oxidative stress via glutathione redox system. Tissue glutathione depletion seems to be responsible for induction of lipid peroxidation (Meis ter and Anders on, 1983). S. nux vomica extract significantly suppressed the depletion of GSH by aerobic oxidation as well as in presence FeSO4 (Figure 2). This indicated that S. nux vomica provides a type of non-enzymatic reducing agent in the system which spares the reduced glutathione from undergoing oxidation.

The biggest doubt, which antioxidants raise, is that of suicidal oxidative stress, induced by certain antioxidants (Koshy et al., 2003; Cao et al., 1997; Offer et al., 2000). These antioxidants can act as prooxidants in certain conditions like presence of transition metals (Koshy et al., 2003; Cao et al., 1997) or at high concentrations (Offer et al., 2000) and can cause the cell to undergo severe oxidative stress ultimately resulting in suicidal cell death. As S. nux vomica possess potent metal chelation property and lack the redox property, it can not act as a prooxidant and can be considered as a safe antioxidant (Tripathi and Chaurasia, 2000).

Alkaloids are the main bioactive ingredients in S. nux vomica, 80% of which are strychnine and brucine, as well as their derivatives such as brucine N-oxide or isostrychnine (Cai et al., 1990). The antioxidant and metal chelation property of strychnine and brucine have been reported by Tripathi and Chaurasia (2000). In view of the recent animal studies strongly suggesting anti-inflammatory role of alkaloids (Barbosa-Filho et al., 2006), the anti-inflammatory activity of S. nux vomica may be explained due to presence of alkaoids.

Conclusion

The results of this study show that Stychnos nux vomica Linn. extract has anti-inflammatory activity against early phase (acute paw edema), late phase (cotton pellet granuloma) of inflammation without any deleterious side effects. The anti-inflammatory activity could be attributed to the presence of alkaloids, and other related s ynergis tic components with antioxidant and metal chelation property.

Acknowledgement

Author is thankful to Department of Medicinal Chemistry, Institute of Medical Sciences, Banaras Hindu University, Varanasi, India for extending research facilities.

References

Bailey, P.J., 1988. Sponge implants as models. Methods Enzymol, 162: 327-334.

Barbosa-Filho J.M., M.R. Piuvezam, M.D. Moura, M.S. Silva, K.V.B. Lima, E.V.L. da-Cunha, I.M. Fechine and O.S. Takemura, 2006. Anti-inflammatory activity of alkaloids. a twenty-century review. Rev. Bras. Farmacogn., 16(1): 109-139.

Bhanu, M.N. and T.N. Vasudevan, 1988. Studies on sodhana of nux vomica. Indian Drugs, 26: 150-152.

Bucher, J.R., M. Tien, L.A. Morehouse and S.D. Aust, 1983. Redox Cycling and Lipid Peroxidation: The Central Role of Iron Chelates. Fundam. Appl. Toxicol., 3: 222-226.

Cai, B.C., M. Hattori and T. Namba, 1990. Processing of nux vomica. II. Changes in alkaloid composition of the seeds of Strychnos nux-vomica L. on traditional drug-processing. Chem. Pharm. Bull., 38: 1295-1298.

Cao G., E. Sofic and R.L. Prior, 1997. Antioxidant and proxidant behaviour of flavonoids structure activity relationship. Free Rad. Biol. Med., 22: 749-760.

Chaurasia, S., P. Tripathi and Y.B. Tripathi, 1995. Antioxidant and anti-inflammatory property of Sandhika : a compound herbal drug. Ind. J. Exp. Biol., 33: 428-432.

Choudhury, R.C., 1977. Role of some indigenous drugs in Sandhigata vata. Rheumatism, 13(1): 10-15.

Conner, E.M. and M.B. Gris ham, 1996. Inflammation, free radicals, and antioxidants. Nutrition, 12: 274-277.

Ellman, G.L., 1959. Tis s ue sulphydril groups. Arch. Biochem. Biophys, 82: 70-77.

Halliwell, B., 1987. Oxygen radicals and metal ions: potential antioxidant intervention strategies. Ann. Intern. Med., 107: 526-45.

Halliwell, B. and J.M.C. Gutteridge, 1999. Free radicals in biology and medicine, Oxford University press.

Hogeberg, J., S. Orrenius and R.E. Lars on, 1975. Lipid peroxidation in isolated hepatocytes. Eu. J. Biochem., 50: 595-602.

Jain, S.K. and R.A. DeFilipps, 1991. In Medicinal Plants of India. Reference Publications, Algonac, Michigun, 1: 392-393.

Koshy H., B.S. Dwarkanath, H.G. Raj, R. Chandra and T L. Mathew, 2003. Suicidal by certain antioxidants. Ind. J. Exp. Biol., 41: 1273-1278.

Lowery, O.H., N.J. Roserbrough, A.L. Farr and J.R. Randoll, 1951. Protein measurement with Folin Phenol reagent. J. Biol. Chem., 193: 265-275.

Mahajan, A. and V.R. Tandon, 2004. Antioxidants and rheumatoid arthritis. J. Indian Rheumatol. As soc., 12: 139-142.

Masilamani, G., T.P.R. Bharadwaj and K.K. Purushothaman, 1979. Role of etti ennei and nanguneri ennei in the treatment of Karappan (Eczema)--A pilot study. J. Res. Indian Med. Yoga Homoeop., 14: 74-80.

Masilamani, G., A. Showkath and V. Subbalakshmi, 1981. Study on Karappan (Eczema). J. Res. Ayur. Siddha, 2(2): 109-121.

Mukhopadhyay, A. and S.C. Lahiri, 1992. Evaluation of some newer non-steroidal anti-inflammatory indan-1 acids in various biological systems. Indian J. Exp. Biol., 30(7): 583-586.

Murthy, K.S., P.C. Sharma and P. Kishore, 1986. Tribal remedies for snakebite from Orissa. Ancient Sci. Life, 6: 122-123.

Okhawa, H, W.Ohishi and K. Yagi, 1979. Assay formulation lipid peroxides in animal tissues by thiobarbituric acid reaction, Anal. Biochem., 95: 351-358.

Offer T., A. Russo, A. Samuni, 2000. The prooxidative activity of SOD and nitroxide SOD mimics. FASEB J., 14: 1215-1223.

Pandey, S., M. Sharma, P. Chaturvedi and Y.B. Tripathi, 1994. Protective effect of R. cordifolia on lipid peroxide formation in isolated liver homogenate. Ind. J. Exp. Biol., 32: 180-183.

Parke, D.V. and A. Sapota, 1996. Chemical toxicity and reactive oxygen species. Int. J. Occup. Med. Environ. Health, 9(4): 331-340.

Reitman, S. and S. Frankel, 1957. A colorimetric method for determination of SGOT and SGPT. Am. J. Clin. Path., 28: 56-63.

Sen, R., D.C. Pal and A.M. Saren, 1983. Traditional uses and ethnobotany of Kuchila. J. Econ. Tax. Bot., 5: 533-537.

Shukla, K.P., S.P. Singh, N. Kishore, D.R. Singh and S. Srivastava, 1985. Evaluation of ras nadi guggulu compound in the treatment of rheumatoid arthritis. Rheumatis m, 21: 16-25.

Spector W.G., 1969. The granulomatous inflammatory exudate. Int. Rev. Exp. Pathol., 8: 1-55.

Suleyman, H., L.O. Demirezer, A. Kuruuzum, Z.N. Banoglu, F. Gocer and G. Ozbakir, 1999. Antiinflammatory effect of the aqueous extract from Rumex patientia L. roots J. Ethnopharmacol., 65: 141-148.

Svingen, B.A., J.A. Buege, F.O. O'Neal and S.D. Aust, 1979. The mechanism of NADPH-dependent lipid peroxidation. The propagation of lipid peroxidation. J. Biol. Chem., 254(13): 5892-5899.

Swingle, K.F. and F.E. Shideman, 1 972. Phases of the inflammatory response to subcutaneous implantation of a cotton pellet and their modification by certain antiinflammatory agents. J. Pharmacol. Exp. Ther., 183(1): 226-234.

Thakur, R.S., H.S. Puri and A. Husain, 1989. In Major Medicinal Plants of India. Central Institute of Medicinal and Aromatic Plants, Lucknow, India, pp. 471-474.

Tripathi, Y.B. and S. Chaurasia, 1996a. Effect of Strychnos nux vomica alcohol extract on lipid peroxidation in rat liver. Int. J. Pharmacognos y, 34(4): 295-299.

Tripathi, Y.B. and S. Chaurasia, 1 996b. Studies on the inhibitory effect of Strychnos nux vomica alcohol extract on iron induced lipid peroxidation. Phytomedicine, III(2): 175-180.

Tripathi, Y.B. and S. Chaurasia, 2000. Interaction of Strychnos nux vomica products and iron: with reference to lipid peroxidation. Phytomedicine, 7(6): 523-528.

Vinegar R., W. Schreiber and R. Hugo, 1969. Biphasic development of carrageenin edema in rats. J. Pharmacol. Exp. Ther., 166: 96-103.

Warrier, P.K., V.P.K. Nambiar and C. Ramankully (eds.), 1996. In Indian Medicinal Plants, a compendium of 500 s pecies. Orient Longman Ltd., Madras, India, 5: 202-206.

Winrow, V.R., P.G. Winyard, C.J. Morris and D.R. Blake, 1993. Free radicals in inflammation: second messengers and mediators of tissue destruction. British Medical Bulletin, 49: 506-522.

Winter, C.A., E.A. Risley and G.W. Nuss, 1962. Carrageenan induced oedema in hind paw of the rats as an as say for anti-inflammatory drugs. Proc. Soc. Exp. Bio Med., 111: 544-547.

Savita Chaurasia

Department of Biotechnology, College of Engineering and Technology, IILM Academy of Higher Learning, 17, 18 Knowledge Park II, Greater Noida-201306, Uttar Pradesh, India.

Savita Chaurasia, Anti-inflammatory & Antioxidant Activity of Strychnos Nux Vomica Linn, Am.-Eurasian J. Sustain. Agric., 3(2): 244-252, 2009

Corresponding Author: Dr. Savita Chaurasia, Assistant Professor, Department of Biotechnology, CET, IILM Academy of Higher Learning, 18, Knowledge Park II, Greater Noida-201306, G.B. Nagar, U.P. India. Ph: +911202320056 Fax: +911202320058 E-mail: drsav16@rediffmail.com
Table 1: Effect of Strychnos nux vomica on cotton pellet granuloma.

Group        Dose              Sub group 1

             ([kg.sup.-1]bw)   Cotton weight               % Inhibi-
                               (mg)                        tion

Control      10 ml             30.07  [+ or -]  1.07       --

Strychnos    50 mg             28.66  [+ or -]  0.86 (b)   7.02
nux vomica   100 mg            27.03  [+ or -]  1.02 (a)   15.14
             150 mg            25.65  [+ or -]  0.69 (a)   22.02
             200 mg            24.02  [+ or -]  0.90 (a)   30.14

Group        Dose              Sub group 2

             ([kg.sup.-1]bw)   Cotton weight               % Inhibi-
                               (mg)                        tion

Control      10 ml             30.07  [+ or -]  1.07       --
Strychnos    50 mg             26.67  [+ or -]  0.71 (a)   16.94
nux vomica   100 mg            23.18  [+ or -]  0.84 (a)   34.32
             150 mg            20.04  [+ or -]  0.43 (a)   49.97
             200 mg            17.79  [+ or -]  1.08 (a)   61.18

Group        Dose              Sub group 3

             ([kg.sup.-1]bw)   C otton weight              % Inhibi-
                               (mg)                        tion

Control      10 ml             30.07  [+ or -]  1.07       --
Strychnos    50 mg             23.74  [+ or -]  1.13 (a)   31.53
nux vomica   100 mg            19.43  [+ or -]  0.91 (a)   53.01
             150 mg            15.97  [+ or -]  0.82 (a)   70.25
             200 mg            12.60  [+ or -]  0.72 (a)   87.04

Each value represent mean   [+ or -]  SD (n=6).

Statistical comparison with control group, which received only
drug vehicle (tween 80:water, 1:9).

P value : (a) < 0.001; (b) < 0.05

SG1: Animals were not pretreated with any drug. After implantation
of cotton pellets, drug was given orally for seven days.

SG2 and SG3: Animals were pretreated with drug for 7 and 21 days
respectively and then cotton pellets were implanted and drug
administration was continued for next seven days.

Table 2: Effect of Strychnos nux vomica on serum transaminases.

Group          Dose              SGPT (IU/ml)

               ([kg.sup.-1]bw)   15 days

Control        10 ml             33.22 [+ or -] 6.57
Drug vehicle   10 ml             32.11 [+ or -] 4.67 (b)
Strychnos      50 mg             30.91 [+ or -] 3.03 (b)
nux vomica     100 mg            32.63 [+ or -] 3.98 (b)
               150 mg            32.29 [+ or -] 4.77 (b)
               200 mg            33.97 [+ or -] 5.31 (b)

Group          Dose              SGPT (IU/ml)

               ([kg.sup.-1]bw)   30 days

Control        10 ml             32.27 [+ or -] 5.69
Drug vehicle   10 ml             27.99 [+ or -] 4.88 (b)
Strychnos      50 mg             30.37 [+ or -] 6.24 (b)
nux vomica     100 mg            29.30 [+ or -] 3.92 (b)
               150 mg            28.67 [+ or -] 4.86 (b)
               200 mg            28.43 [+ or -] 5.01 (b)

Group          Dose              SGOT (IU/ml)

               ([kg.sup.-1]bw)   15 days

Control        10 ml             76.39 [+ or -] 5.01
Drug vehicle   10 ml             74.97 [+ or -] 4.01 (b)
Strychnos      50 mg             73.37 [+ or -] 4.92 (b)
nux vomica     100 mg            75.61 [+ or -] 3.67 (b)
               150 mg            75.92 [+ or -] 4.03 (b)
               200 mg            75.21 [+ or -] 3.92 (b)

Group          Dose              SGOT (IU/ml)

               ([kg.sup.-1]bw)   30 days

Control        10 ml             76.91 [+ or -] 5.82
Drug vehicle   10 ml             74.54 [+ or -] 3.88 (b)
Strychnos      50 mg             73.13 [+ or -] 5.16 (b)
nux vomica     100 mg            75.41 [+ or -] 4.90 (b)
               150 mg            74.69 [+ or -] 3.82 (b)
               200 mg            74.08 [+ or -] 4.98 (b)

Each value represent mean  [+ or -] SD (n=6).

Statistical comparison with control group, which received only,
distilled water.

P value: (b) = NS (not significant)

Table 3: Effect of Strychnos nux vomica on lipid peroxidation.

S. nux vomica   TBARS (nmoles/100mg protein)    [Fe.sup.3+]-ADP
([micro]g/ml)   FeS[O.sub.4]

00              446.54 [+ or -] 6.41            477.82 [+ or -] 7.98
25              352.16 [+ or -] 7.52 (a)        328.33 [+ or -] 9.42
50              315.33 [+ or -] 6.68 (a)        302.37 [+ or -] 8.65
100             272.50 [+ or -] 6.59 (a)        266.56 [+ or -] 7.96
200             235.16 [+ or -] 3.97 (a)        223.67 [+ or -] 8.31
400             164.21 [+ or -] 3.94 (a)        149.24 [+ or -] 7.32
800             073.94 [+ or -] 4.94 (a)        069.84 [+ or -] 5.67

Each value represent mean [+ or -] SD (n=6).

Statistical comparison with control value, which was arrived by
adding 0.5mM FeS[O.sub.4] and (1.6 mM-62 [micro]M) [Fe.sub.3+]-ADP
for 30 minutes.

P value: a < 0.001

Table 4: Comparative study of S. nux vomica with Vitamin E and
parabenzoquinone

Antioxidant        [ED.sub.50] ([micro]g/ml)
                   FeS[O4.sub.]               [Fe.sup.3+]-ADP

S. nux vomica      149                        85
Vitamin E          58                         12
Parabenzoquinone   35                         10

These data are best representative of six separate experiments.
COPYRIGHT 2009 American-Eurasian Network for Scientific Information
No portion of this article can be reproduced without the express written permission from the copyright holder.
Copyright 2009 Gale, Cengage Learning. All rights reserved.

Article Details
Printer friendly Cite/link Email Feedback
Title Annotation:Original Articles
Author:Chaurasia, Savita
Publication:American-Eurasian Journal of Sustainable Agriculture
Article Type:Report
Geographic Code:9INDI
Date:May 1, 2009
Words:5002
Previous Article:An ethnobotanical survey of Jessore district in Khulna Division, Bangladesh.
Next Article:Ethnobotanical survey of the Tripura tribe of Bangladesh.
Topics:

Terms of use | Privacy policy | Copyright © 2019 Farlex, Inc. | Feedback | For webmasters