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Hepatoprotective and antioxidant activity of N-Trisaccharide in different experimental rats.


Imbalance between reactive oxygen species and antioxidant defense systems lead to chemical modifications of biologically relevant macromolecules and cellular components, such as lipids, proteins and DNA. This imbalance initiates a logical pathobiochemical mechanism for the initiation and development of several diseases. It is believed that several diseases, such as cancer, diabetes, ageing, hypertension, obesity, cardiac dysfunction and other degenerative diseases in humans which involve oxidative processes are mediated by free radicals (Pennathur et al. 2007; Olayinka and Bernard 2010).

Diabetes is usually accompanied by increased generation of free radicals. Implication of oxidative stress in pathogenesis of diabetes is due to non-enzymatic protein glycosylation, auto oxidation of glucose, impaired antioxidant enzyme and formation of peroxides. Lipid peroxidation is a key marker of oxidative stress that results in extensive membrane damage and dysfunction (Parisa et al. 2007). Hyperglycemia and hyperlipidemia are two important characters of diabetes mellitus (DM), an endocrine based disease. Diabetes is a complex and heterogeneous disorder affecting more than 100 million people worldwide and causing serious socioeconomic problems (Srinivasan and Ramarao 2007). It is now well established that hyperlipidemia represents a major risk factor for the premature development of atherosclerosis and its cardiovascular complications (Kaur et al. 2002), such as heart and blood vessel diseases. To avoid this, controlling not only blood glucose levels but also lipid levels are necessary (Markuszewski et al. 2006). Earlier work in our laboratory has shown that N-Trisaccharide, isolated from Cucumis prophetarum has significant antihyperglycemic activity (Kavishankar and Lakshmidevi 2014). The present study was taken up to identify the protective effect of N-Trisaccharide on different experimental rats.

Materials and methods

Isolation of active compound

The active compound was isolated via a novel one-step precipitation process. The compound was precipitated with the addition of methanol: water (4:1) to the crude extract, centrifuged at 5000 rpm for 5 min to separate the supernatant layer. The white precipitate was washed twice with methanol and dried using lyophilizer to obtain water soluble compound. The structure was elucidated using NMR, LC-MS/MS, IR and HPLC-DAD experiments (Kavishankar and Lakshmidevi 2014).

Experimental design

Albino wistar rats of either sex, weighing 150-180g were used. Animals were maintained at 22 [+ or -] 2[degrees]C with 12 h light and dark cycle, fed on standard pellet diet supplied by Lipton India Ltd. Animals had free access to diet and water. All animal studies conducted were approved by the Institutional Animal Ethics Committee, University of Mysore (Approval No. UOM/IAEC/4/2012), Mysore, as stated by prescribed guidelines of Committee for the Purpose of Control and Supervision of Experiments on Animals (CPCSEA), Government of India.

Protocol 1: The hepatoprotective effect of N-Trisaccharide was tested using C[Cl.sub.4] model. The animals were randomly divided into five groups, each consisting of six animals. Group-I (normal control) received normal saline solution orally (0.2 ml/100 g); Group-II (induction control) was given a single intraperitoneal dose of C[Cl.sub.4] (2.0g/kg b.w). Group-III served as positive control and received orally 25mg/kg b.w of silymarin. Group-IV and V received N-Trisaccharide at 25 and 50mg/kg b.w orally, respectively. All the groups were treated for 28 consecutive days. At the end of the experiment, animals were sacrificed under ether anaesthesia. Blood samples were collected in centrifuging tubes and allowed to clot for 30 min at room temperature. The obtained serums were taken for assessment of hepatoprotective enzymes and renal function markers. The liver was excised from the animal and immediately processed for histopathological studies. Protocol 2: Type-2 diabetes was experimentally induced according to the method as described by Masiello et al. (1998). Animals with marked hyperglycemia (fasting blood glucose [greater than or equal to] 250 mg/dl), 48 h after STZ-NA treatment were selected for the study. A total of 30 rats were divided into five groups in as follows; group I consisting of normal control rats orally administered N-Trisaccharide (50 mg/kg/b/w); group II was considered as diabetic control; group III and IV were treated with N-Trisaccharide (25 and 50 mg/kg.b.w) respectively; group V was orally treated with standard antidiabetic drug glibenclamide (25 mg/kg/b.w). The treatment was carried out daily for 28 days by gastric intubation with a force feeding needle. All the five groups were sacrificed after an overnight fasting by cervical dislocation. Blood was drawn from the heart. Liver and kidney were removed, washed with chilled saline. Ten percent homogenate (w/v) of liver and kidney was prepared in 150 mM KC1 using homogenizer at 4[degrees]C. The homogenates were centrifuged at 3000 x g for 15 min at 4[degrees]C. The supernatants were frozen at -20[degrees]C until assayed for different enzymes. Blood serum was separated for measuring lipid profile.

DNA fragmentation analysis

DNA fragmentation was assessed by the method of Wang et al. (2007) with slight modifications. Briefly, the liver tissue was homogenized in lysis buffer (pH 8.0) containing 100mM Tris, 20 mM EDTA and 0.8% SDS. Proteinase K (0.4 [micro]g/ml) was added and incubated at 50[degrees]C for 3h. Then mixed with phenol: chloroform: isoamyl alcohol (25:24:1) and centrifuged at 13,000 rpm for 10 min. The resulting aqueous phase was added with 2 volumes of ice-cold absolute ethanol, 1/10th volume of 3 M sodium acetate and incubated for 30 min on ice. DNA was pelleted by centrifuging at 13,000 rpm for 10 min at 4[degrees]C and after separating supernatant, pellet was washed with 1 ml of 70% ethanol. The extracted DNA was resuspended in Tris-EDTA buffer and electrophoretically separated on 1.5% agarose gel, stained with ethidium bromide. The DNA pattern was examined by ultraviolet transillumination.

Biochemical measurements

SGOT and SGPT activities were determined by the method of Reitman and Frankel (1957). Serum ALP activity was determined by p-nitro phenyl phosphate method (Bessey et al. 1946). Serum urea and creatinine were measured by the diacetyl monoxime method (Wybenga et al. 1971) and Jaffe's method (Slot 1965), respectively. Glutathione was estimated colorimetrically by using DTNB as described by Ellman (1959). Ascorbic acid and alpha tocopherol, the non-enzymatic antioxidants were estimated according to the methods of Omaye et al. (1979) and Baker et al. (1980) respectively. The enzymatic antioxidants glutathione peroxidase, catalase and superoxide dismutase were estimated according to Rotruck et al. (1973), Sinha (1972) and Kakkar et al. (1984) respectively. Serum TG, TC and HDL-C were estimated according to the methods of Zlatkis et al. (1953), Foster and Dunn (1973) and Burstein et al. (1970), respectively. The serum levels of VLDL-C and LDL-C were calculated using Friedewald formula (Friedewald et al. 1972).

Statistical analysis

The experimental data are expressed as mean [+ or -] SD. Statistical comparisons were performed by one-way analysis of variance (ANOVA) followed by Student's t-test. The results were considered statistically significant at p < 0.05.


The effect of N-Trisaccharide on DNA fragmentation was examined in the control and experimental groups (Fig. 1). Rats treated with N-Trisaccharide showed a significant decrease in DNA fragmentation compared with untreated rat, whereas there was no difference in its laddering pattern in the normal rats treated with N-Trisaccharide as compared with control. These observations suggest that N-Trisaccharide treatment appears to significantly suppress the progression of apoptosis in the liver and kidney of CC[L.sub.4] induced rats.

Histopathological results provided supportive evidence for biochemical findings. Histology of liver section of one animal from each group is presented in Fig. 2. Plate-A. Liver section of normal control rat exhibited distinct hepatic cells, the central vein is seen with no visible lesion, sinusoids and epithelium lining are normal, In Plate-C, C[Cl.sub.4] induced liver damage shows total loss of hepatic architecture, necrosis, lymphocyte infiltration, loss of cellular boundaries, and joining together of nucleus. In addition, congestion of sinusoids, Kupffer cell hyperplasia, crowding of central vein and apoptosis are also evident. Rats treated with silymarin (Plate-F) show less necrosis and almost normal liver architecture with no obvious necrosis as compared to C[Cl.sub.4] treated rats section (Plate-C). Sections of Plate-E and F treated groups with N-Trisaccharide (25 and 50 mg/kg) show gradual recovery of hepatic architecture. The central vein is seen and the sinusoids are having hepatitis alteration. Only very slight lymphocyte infiltration is observed in Plate-D. These sections are nearly comparable to the silymarin treated group.

The mechanism by which N-Trisaccharide offers protection against CCLj-induced liver damage could be due to inducing microsomal enzymes either by accelerating the detoxification and excretion of CC14 or by inhibition of lipid peroxidation through inhibition of cytochrome P-450 aromatase favouring liver regeneration.

The effect of N-Trisaccharide on the activities of hepatic (SGOT, SGPT and ALP) and the levels of renal function markers (urea and creatinine) in different experimental group of rats is shown in Fig. 3 and Table 1 respectively. The activities of SGOT, SGPT and ALP were increased significantly in C[Cl.sub.4] untreated group. Administration of N-Trisaccharide significantly decreased (p<0.05) the levels of SGOT, SGPT, ALP, and, urea and creatinine in treated rats compared to those in untreated rats.

Increased levels of serum lipids of TG, TC, HDL-C, LDL-C and VLDL-C of the experimental groups of animals are shown in Fig. 4. The serum lipid levels were significantly higher in untreated diabetic group. After treatment, N-Trisaccharide showed significant reversal compared to untreated diabetic group.

The enzymatic antioxidant levels in liver and kidney are shown in Table 2 and 3 respectively. Lipid peroxide content increased significantly (p < 0.05) in diabetic untreated group compared to normal group. Administration of N-Trisaccharide and glibenclamide for 28 days reversed the high levels back to near normal. The level of enzymatic antioxidants such as CAT, SOD and GPx in liver and kidney of diabetic untreated rats were significantly (p<0.05) lower compared to normal group. Treatment of N-Trisaccharide reverted back the enzyme activities to near normal. Table 4 and 5 illustrate the level of non-enzymatic antioxidants. The levels of GSH, Vit A and Vit E in both liver and kidney were significantly reduced (p < 0.05) in diabetic rats compared to normal rats. Administration of N-Trisaccharide or glibenclamide for 28 days to diabetic rats significantly (p<0.05) restored the level back to near normal.

In all the experimental parameters, treatment of N-Trisaccharide in normal rats showed no adverse effects. Treatment of diabetic rats with N-Trisaccharide at a dose of 25 mg/kg.b.w showed significant (p< 0.05) effect on lipid level, oxidation stress and, hepatic and renal function markers.


DNA fragmentation occurs massively due to oxidative stress and increased fragmentation may enhance apoptotic cell death in liver and kidney. Significant DNA strand break and mutations were earlier reported by Imaeda et al. (2002) and Schmezer et al. (1994) respectively. In our present study, we observed increased DNA fragmentation in liver. Treatment with N-Trisaccharide and silymarin significantly reduced DNA fragmentation in liver of rats.

The possible hepatoprotective activity of N-Trisaccharide in carbon tetrachloride induced hepatotoxicity has been demonstrated. CC14 is a well-known hepatotoxin exerts hepatotoxic effects by generating free radicals in the experimental study of liver disease (Shenoy et al. 2001). It is extensively studied as a liver toxicant, and its metabolites such as trichloromethyl radical (C[Cl.sub.3] S) and trichloromethyl peroxyl radical (C[Cl.sub.3][O.sub.2] S) are reported to be involved in the pathogenesis of liver (Recknagel 1967). These free radicals produced by cytochrome P450 system through biotransformation of C[Cl.sub.4] covalently bind to cell membranes and organelles to elicit lipid peroxidation (Recknagel et al. 1989) by interacting with phospholipids structure and thereby destroying the organ structure (Gilet al. 2000).

Measurement of hepatic function markers (SCOT, SGPT and ALP) is of clinical and toxicological importance as changes in their level are indicative of tissue damage in disease conditions or hepatic dysfunction. Higher release of these enzymes from the cells are indicative of cellular leakage and loss of functional integrity of the cell membrane in liver (Drotman and Lawhorn 1978) and this could be as a result of hepatocyte necrosis or abnormal membrane permeability. SGOT is a sensitive indicator of acute liver damage and elevation of this enzyme in non-hepatic diseases is unusual. SGPT is more selectively a liver parenchymal enzyme than SGOT (Shah 2002). The elevated levels of these marker enzymes in the current study were observed in C[Cl.sub.4] intoxicated rats. However, during the investigation, reduction of SGOT, SGPT and SALP concentrations were observed due to the influence of N-Trisaccharide.

The histological observations of liver of rats induced by C[Cl.sub.4] administration provided complementary evidence to prove that treatment with N-Trisaccharide attenuated the cytoplasmatic changes. This effect could be attributable to the antioxidant activity of N-Trisaccharide, which attenuated the oxidative threat caused by C[Cl.sub.4] and restored normal physiological functions.

Disturbances in glucose metabolism, altered lipid levels and oxidative stress are important risk factors for diabetes. Insulin deficiency causes a variety of derangements in metabolic and regulatory processes, which in turn leads to accumulation of lipids such as TG and TC in diabetic patients (Goldberg 1981). Hyperglycemia is accompanied with dyslipidemia (Bierman et al. 1996), a condition which is characterized by increase in TG, TC, LDL, VLDL and fall in HDL representing risk factor for coronary heart diseases. This abnormal high level of serum lipids causes lipolytic harmones its uninhibited actions on fat depots. Under normal conditions, lipoprotein lipase hydrolyses triglycerides, thereby maintaining normal lipid profile. However, this enzyme is not activated in diabetic state due to insulin deficiency resulting in hypertriglyceridemia (Pushparaj et al. 2007) and due to metabolic abnormalities; it is also associated with hypercholesterolemia (Murali et al. 2002). In the present study, N-Trisaccharide significantly reversed the serum lipid level towards normal by increasing the level of HDL cholesterol. High levels of TC and particularly LDL-C are the predictors of atherosclerosis (Temme et al. 2002) and treatment with N-Trisaccharide markedly reduced both serum TG and LDL levels.

Earlier studies in our laboratory have shown that N-Trisaccharide of Cucumis prophetarum (L.) at 50mg/kg.b.w possesses significant antihyperglycemic activity, which is due to increased insulin secretion from pancreatic [beta]-cells, as it is evident by the histological studies that shows the restoration of [beta]-cells from islets of Langerhans (Kavishankar and Lakshmidevi 2014).

The imbalance in the homeostatic phenomena between oxidants and antioxidants in the body could be due to hyperphysiological burden of free radicals. Hyperglycemia increases the generation of free radicals by glucose auto-oxidation and the increment of free radicals may lead to liver and kidney damage (Yadav et al. 2000). A notable increase in lipid peroxidation in the liver and kidney was observed in diabetic rats. The level of lipid peroxidation (TBARS) and Reactive oxygen species (superoxide anion, hydrogen peroxide and hydroxyl radical) are common markers of oxidation stress in diabetes. The production of these radicals can cause tissue damage by reacting with polyunsaturated fatty acids in the lipid bi-layer (Dass Vashist et al. 2000; Scheuer et al. 2000). Treatment with N-Trisaccharide reduced lipid peroxidation markers to near normal levels in diabetic rats.

An increased level of TBARS was observed in diabetic rats and administration of N-Trisaccharide significantly reduced these levels. Catalase (CAT) catalyzes the reduction of hydrogen peroxide and protects tissues from highly reactive hydroxyl radicals (Chance et al. 1952). A reduced level of CAT was observed in diabetic rats and administration of N-Trisaccharide increased the level to near normal. Superoxide dismutase (SOD) catalyzes the conversion of superoxide anion to hydrogen peroxide and oxygen (Selvan et al. 2008). In diabetic rats, reduced level of SOD was observed and treatment with N-Trisaccharide markedly increased the level to near normal.

Detoxification of hydrogen peroxide to water through oxidation of reduced glutathione is mediated by glutathione peroxidase (GPx) (Freeman and Crapo 1982). An increased GPx activity was observed after the administration of N-Trisaccharide compared to untreated diabetic rats. Glutathione is an important intracellular peptide that exhibits multiple functions ranging from antioxidant defense to modulation of cell proliferation (Lu 1999). Vit A acts as a powerful free radical scavenger for singlet oxygen (Krishnakumar et al. 1999) and contributes to the inhibition of lipid peroxidation by promoting the recycling of Vit E (Kumar et al. 2005). A decreased level of reduced glutathione (GSH), Vit A and Vit E was observed in diabetic untreated rats and treatment with N-Trisaccharide reversed the levels to near normal. Also, a significant increase in the level of urea and creatinine in the serum was observed in diabetic rats, which are considered as markers of renal dysfunction (Bethesda 2001). Administration of N-Trisaccharide significantly reduced the levels of serum urea and creatinine in treated rats.

The result of the present investigation indicates that N-Trisaccharide isolated from Cucumis prophetarum (L.) possess antioxidant, antihyperlipidemic, hepato and renal protective properties in different experimental rats.

Conflict of interest



Article history:

Received 30 January 2014

Accepted 20 April 2014


The authors are thankful to University Grants Commission F.NO.39-223/2010 (SR) for providing financial assistance.


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G.B. Kavishankara (a,b), S.S. Moreeb, N. Lakshmidevi (a) *

(a) Department of Studies in Microbiology, University of Mysore, Mysore 570006, India

(b) Department of Studies in Biochemistry, University of Mysore, Mysore 570006, India

* Corresponding author. Tel.: +91 90081 77435.

E-mail address: (N. Lakshmidevi).


Table 1 Effect of N-Trisaccharide on serum urea and creatinine
in normal and experimental diabetic animals.

Groups            Urea                        Creatinine

Normal            41.22 [+ or -] 2.27 (a)     0.61 [+ or -] 0.0363 (a)
Normal + N-       41.54 [+ or -] 1.92 (b)     0.61 [+ or -] 0.03 (b)
  (50 mg/kg)
Diabetic          68.33 [+ or -] 1.21         0.71 [+ or -] 0.036
Diabetic + N-     51.18 [+ or -] 1,59 (b,c)   0.62 [+ or -] 0.057 (b)
  (25 mg/kg)
Diabetic + N-     58.83 [+ or -] 2.22 (b,c)   0.60 [+ or -] 0.028 (b)
  (50 mg/kg)
Diabetic +        62.79 [+ or -] 3.07 (b,c)   0.61 [+ or -] 0.043 (b)
  (25 mg/kg)

Values are mean [+ or -] SD (n = 6). Values not sharing a common
superscript differ significantly at p < 0.05.

Table 2 Effect of N-Trisaccharide on lipid peroxidation and enzymatic
antioxidants in liver of normal and experimental diabetic animals.

Groups               Lipid peroxidation               CAT

Normal             2.75 [+ or -] 0.22 (a)    60.5 [+ or -] 1.76 (a)

Normal + N-        2.73 [+ or -] 0.25 (b)    60.5 [+ or -] 1.23 (b)

(50 mg/kg)

Diabetic             5.23 [+ or -] 0.56       35.66 [+ or -] 1.16

Diabetic + N-       4.75 [+ or -] 0.39       43.25 [+ or -] 2.09
Trisaccharide              (b,c)                     (b,c)

(25 mg/kg)

Diabetic * N-         3.4 [+ or -] 0.43      56.07 [+ or -] 1.15
Trisaccharide              (b,c)                     (b,c)

(50 mg/kg)

Diabetic +           4.78 [+ or -] 0.39          66 [+ or -] 1.27
glibenclamide              (b,c)                     (b,c)

(25 mg/kg)

Groups                      GPx                       SOD

Normal             0.36 [+ or -] 0.02 (a)   33.91 [+ or -] 0.9l (a)

Normal + N-        0.35 [+ or -] 0.02 (b)   31.91 [+ or -] 1.49 (b,c)

(50 mg/kg)

Diabetic             0.16 [+ or -] 0.02       17.86 [+ or -] 1.30

Diabetic + N-       0.20 [+ or -] 0.02        22.58 [+ or -] 1.1l
Trisaccharide              (b,c)                      (bc)

(25 mg/kg)

Diabetic * N-        0.31 [+ or -] 0.02       27.36 [+ or -] 1.31
Trisaccharide              (b,c)                     (b,c)

(50 mg/kg)

Diabetic +          0.31 [+ or -] 0.02        25.68 [+ or -] 1.17
glibenclamide              (b,c)                     (b,c)

(25 mg/kg)

Values are mean [+ or -] SD (n = 6).

Values not sharing a common superscript differ
significantly at p < 0.05.

Table 3 Effect of N-Trisaccharide on lipid peroxidation and
enzymatic antioxidants in kidney of normal and experimental
diabetic animals.

Groups            Lipid peroxidation        CAT

Normal            3.17 [+ or -] 0.29 (a)    51.35 [+ or -] 1.84 (a)

Normal + N/       2.98 [+ or -] 0.13 (b)    51.02 [+ or -] 1.65 (b)

(50 mg/kg)

Diabetic          6.01 [+ or -] 0.27        27 [+ or -] 1.04

Diabetic +        5.03 [+ or -] 0.36 (b,c)   40.91 [+ or -] 1.28 (b,c)

(25 mg/kg)

Diabetic +        4.65 [+ or -] 0.56 (b,c)   48.33 [+ or -] 1.77 (b,c)

(50 mg/kg)

Diabetic +        4.78 [+ or -] 0.41 (b,c)   48.83 [+ or -] 2.06 (b,c)

(25 mg/kg)

Groups            GPx                       SOD

Normal            0.27 [+ or -] 0.033       21.33 [+ or -] 1.213

Normal + N/       0.30 [+ or -] 0.03 (b)    21.41 [+ or -] 1.02 (b)

(50 mg/kg)

Diabetic          0.13 [+ or -] 0.03        14.25 [+ or -] 1.08

Diabetic +        0.16 [+ or -] 0.01 (b,c)  16.53 [+ or -] 1.07 (b,c)

(25 mg/kg)

Diabetic +        0.25 [+ or -] 0.01 (b,c)  18.86 [+ or -] 1.27 (b,c)

(50 mg/kg)

Diabetic +        0.29 [+ or -] 0.01 (b)    18.58 [+ or -] 1.1 l (b,c)

(25 mg/kg)

Values are mean [+ or -] SD (n = 6). Values not sharing a common
superscript differ significantly at p < 0.05.

Table 4 Effect of N-Trisaccharide on non-enzymatic antioxidants in
liver of normal and experimental diabetic animals.

Groups                      GSH                        VitC

Normal            4.38 [+ or -] 0.48 (a)      2.71 [+ or -] 0.27 (a)

Normal +          4.31 [+ or -] 0.50 (b)      2.87 [+ or -] 0.37 (b)

(50 mg/kg)

Diabetic            2.43 [+ or -] 0.16          1.87 [+ or -] 0.26

Diabetic +        3.18 [+ or -] 0.29 (b,c)  2.3 [+ or -] 0.2 l (b) (c)

(25 mg/kg)

Diabetic +        4.17 [+ or -] 0.34 (b)      2.80 [+ or -] 0.27 (b)

(50 mg/kg)

Diabetic +        3.80 [+ or -] 0.36 (b,c)    2.41 [+ or -] 0.42 (b)

(25 mg/kg)

Groups                     VitE

Normal            0.83 [+ or -] 0.08 (a)

Normal +          0.82 [+ or -] 0.09 (b)

(50 mg/kg)

Diabetic            0.65 [+ or -] 0.10

Diabetic +        0.72 [+ or -] 0.03 (c)

(25 mg/kg)

Diabetic +        0.78 [+ or -] 0.13 (b)

(50 mg/kg)

Diabetic +        0.81 [+ or -] 0.09 (b)

(25 mg/kg)

Values are mean [+ or -] SD (n = 6). Values not sharing a common
superscript differ significantly at p < 0.05.

Table 5 Effect of N-Trisaccharide on non-enzymatic
antioxidants in kidney of normal and experimental diabetic

Groups                    GSH                  Vit C

Normal            3.41 [+ or -] 0.45    2.40 [+ or -] 0.38
                          (a)                   (a)

Normal +          3.66 [+ or -] 0.41    2.74 [+ or -] 0.33
N-Trisaccharide           (b)                   (b)

(50 mg/kg)

Diabetic          1.63 [+ or -] 0.35    1.29 [+ or -] 0.31

Diabetic +        2.47 [+ or -] 0.44    2.17 [+ or -] 0.37
N-Trisaccharide          (b,c)                  (b)

(25 mg/kg)

Diabetic +        2.73 [+ or -] 0.30    2.42 [+ or -] 0.33
N-Trisaccharide          (b,c)                  (b)

(50 mg/kg)

Diabetic +        2.15 [+ or -] 0.27    1.87 [+ or -] 0.31
glibenclamide            (b,c)                  (b,c)

(25 mg/kg)

Groups                  Vit E

Normal            0.73 [+ or -] 0.13

Normal +          0.71 [+ or -] 0.07
N-Trisaccharide          (a)

(50 mg/kg)

Diabetic          0.59 [+ or -] 0.16

Diabetic +        0.63 [+ or -] 0.12
N-Trisaccharide          (a)

(25 mg/kg)

Diabetic +        0.63 [+ or -] 0.11
N-Trisaccharide          (a)

(50 mg/kg)

Diabetic +        0.66 [+ or -] 0.10
glibenclamide            (a)

(25 mg/kg)

Values are mean [+ or -] SD (n = 6). Values
not sharing a common superscript
differ significantly at p < 0.05.
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Author:Kavishankara, G.B.; Moreeb, S.S.; Lakshmidevi, N.
Publication:Phytomedicine: International Journal of Phytotherapy & Phytopharmacology
Article Type:Report
Date:Jul 15, 2014
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