Protective effect of Indigofera aspalathoides against CCl4-induced hepatic damage in rats

The alcoholic extract of stem of Indigofera aspalathoides was evaluated for its antihepatotoxic activity against CCl(4)-induced hepatic damage in rats. The activity was evaluated by using biochemical parameters, such as serum glutamate pyruvate transaminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT), alkaline phosphatase (ALP), total bilirubin and gama glutamate transpeptidase (GGTP). The histopathological changes of liver sample were compared with respective control. The extract showed remarkable hepatoprotective effect.     

Effect of Indigofera aspalathoides on complete Freund’s adjuvant-induced arthritis in rats

The effect of ethanol extract of stems of Indigofera aspalathoides Vahl (Papilionaceae) (EIA) was evaluated for anti-arthritic activity on complete Freund’s adjuvant-induced (CFA-induced) arthritis in rats. The EIA was administered orally at doses of 250 and 500?mg/kg daily for 30 days. The paw volume was measured on days 7, 14, 21 and 30. At the end of day 30, the rats were sacrificed and various biochemical parameters such as serum aspartate transaminase (AST), alanine aminotransferase (ALT), alkaline phosphatase (ALP), total cholesterol and triglycerides were estimated. Antioxidant enzymes, such as superoxide dismutase (SOD), catalase, glutathione peroxidase (GPx) and lipid peroxide (LPO) in the liver and kidney of normal, arthritic control and EIA treated rats were studied. Oral administration of EIA effectively inhibits rat paw edema in a dose-dependent manner. EIA significantly (P?<0.01) altered the biochemical parameters which were affected in arthritic rats. There was significant alteration in LPO, SOD, catalase, and GPx levels when compared to arthritic control rats. Our findings showed a significant anti-arthritic effect of EIA against CFA-induced arthritis in rats.     

The effects of paeoniflorin on LPS-induced liver inflammatory reactions

Paeoniflorin (PF), a monoterpene glucoside, is a primary bioactive component of paeony, the root extract of Paeonia lactiflora. We tested the antioxidant effects of PF and its ability to prevent lipopolysaccharide (LPS)-induced oxidative stress. We intraperitoneally administered PF (2.5, 5, or 10 mg/kg) to rats for 20 days. On day 21, we injected the rats with LPS 4 h before sacrifice and measured serum levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase as well as the levels of malondialdehyde, superoxide dismutase, catalase, and glutathione peroxidase in liver whole-cell homogenates and mitochondrial fractions. LPS treatment increased levels of glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, lactate dehydrogenase, and malondialdehyde, but PF treatment blocked these increases. LPS treatment also decreased antioxidant levels of superoxide dismutase, catalase, and glutathione peroxidase, but PF blocked these decreases. PF also protected liver tissue, as shown by histopathology. These results suggest that PF can protect against LPS-induced liver inflammation.     

Zingiber officinale Roscoe prevents acetaminophen-induced acute hepatotoxicity by enhancing hepatic antioxidant status.

A large number of xenobiotics are reported to be potentially hepatotoxic. Free radicals generated from the xenobiotic metabolism can induce lesions of the liver and react with the basic cellular constituents - proteins, lipids, RNA and DNA. Hepatoprotective activity of aqueous ethanol extract of Zingiber officinale was evaluated against single dose of acetaminophen-induced (3g/kg, p.o.) acute hepatotoxicity in rat. Aqueous extract of Z. officinale significantly protected the hepatotoxicity as evident from the activities of serum transaminase and alkaline phosphatase (ALP). Serum glutamate pyruvate transaminase (SGPT), serum glutamate oxaloacetate transaminase (SGOT) and ALP activities were significantly (p<0.01) elevated in the acetaminophen alone treated animals. Antioxidant status in liver such as activities of superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase and glutathione-S-transferase (GST), a phase II enzyme, and levels of reduced glutathione (GSH) were declined significantly (p<0.01) in the acetaminophen alone treated animals (control group). Hepatic lipid peroxidation was enhanced significantly (p<0.01) in the control group. Administration of single dose of aqueous extract of Z. officinale (200 and 400mg/kg, p.o.) prior to acetaminophen significantly declines the activities of serum transaminases and ALP. Further the hepatic antioxidant status was enhanced in the Z. officinale plus acetaminophen treated group than the control group. The results of the present study concluded that the hepatoprotective effect of aqueous ethanol extract of Z. officinale against acetaminophen-induced acute toxicity is mediated either by preventing the decline of hepatic antioxidant status or due to its direct radical scavenging capacity.     

Protective Effect of Ethanol Extract of Gymnosporia montana (Roth) Bemth. in Paracetamol-induced Hepatotoxicity in Rats

The aim of the present study was to explore the hepatoprotective activity of the ethanol extract of leaves of Gymnosporia montana (Roth) Bemth. (Family: Celastraceous) against paracetamol-induced hepatotoxicity. Hepatotoxicity in Wistar rats was induced by a single intraperitoneal dose of 500 mg/kg of paracetamol and studied by comparing parameters such as serum glutamate oxaloacetate transaminase, serum glutamate pyruvate transaminase, alkaline phosphatase and histopathological examination of liver. Pre and post-treatment with ethanol extract of Gymnosporia montana (Roth) Bemth. at doses of 50 and 100 mg/kg was studied by comparing the above mentioned parameters with silymarin (100 mg/kg) as standard. Both doses of ethanol extract of Gymnosporia montana (Roth) Bemth. were found to be hepatoprotective. Extract at the dose of 100 mg/kg produced effects comparable to those of silymarin. The present study indicates that alcohol extract of Gymnosporia montana (Roth) Bemth. possessed significant hepatoprotective activity.     

In Vivo prophylactic effects of oleanolic acid isolated from chloroform extract of Flaveria trinervia against ethanol induced liver toxicity in rats

The prophylactic effects of oleanolic acid (OA) isolated from chloroform extract (CE) of Flaveria trinervia against ethanol induced liver toxicity was investigated using rats. CE and OA at three different doses were tested by administering orally to the ethanol treated animals during the last week of the 7 weeks study. Silymarin was used as the standard reference. The substantially elevated serum enzymatic levels of serum glutamate oxaloacetate transaminase, glutamate pyruvate transaminase, alkaline phosphatase and bilirubin in ethanol treated animals were restored towards normalcy by treatment of CE and OA. In vivo antioxidant and in vitro free radical scavenging activities were also positive for all the three concentrations of CE and OA. However, OA at 150 mg/kg showed significant activity when compared to the other two doses. Biochemical observations in support with histopathological examinations revealed that CE and OA possess hepatoprotective action against ethanol induced hepatotoxicity in rats.     

Combined effects of vitamin C, vitamin E, and sodium selenate supplementation on absolute ethanol-induced injury in various organs of rats

In this study, the effect of combination of vitamin C (ascorbic acid), vitamin E (alpha -tocopherol), and selenium (sodium selenate) on ethanol-induced liver and intestine injury in rats was investigated. The ethanol-induced injury was produced by the administration of 1 ml of absolute ethanol to each rats. Animals received vitamin C (250 mg/kg), vitamin E (250 mg/kg), and sodium selenate (Se) (0.5 mg/kg) for 3 days; 1 h after the final antioxidant administration, they were sacrificed. Lipid peroxidation and glutathione levels, catalase (CAT), lactate dehydrogenase (LDH), superoxide dismutase (SOD), and glutathione peroxidase (GP(x)) activities were determined in liver and intestine tissues. Myeloperoxidase (MPO), aspartate transaminase (AST), alanine transaminase (ALT), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT) were determined in liver tissue. Also, CAT activity, urea, creatinine, uric acid, and total lipid levels were determined in serum samples. In the ethanol group, serum urea, creatinine, uric acid, and total lipid levels; liver and intestine LDH; liver MPO, AST, ALP, ALT, and GGT activities; and liver and intestine LPO levels increased, whereas serum CAT activity, liver and intestine GSH levels, and CAT, SOD, and GP(x) activities decreased. On the other hand, treatment with vitamin C, vitamin E, and Se reversed these effects. As a result of these findings, we can say that the combination of vitamin C, vitamin E, and selenium has a protective effect on ethanol-induced changes in lipid peroxidation, glutathione levels, and antioxidant enzyme activities in liver and intestine tissues, and in some serum parameters of rats.     

Hepatoprotective activity of Andrographis Paniculata and Swertia Chirayita

Andrographis paniculata (Family: Acanthaceae) and Swertia chirayita (Family: Gentianaceae) are two controversial medicinal plants used as Kiriyattu, having similar therapeutic action and are used as a hepatoprotective and hepatostimulative agent. A. paniculata grows in southern parts of India and S. chirayita in the Himalayan region. The present work concerns on the ability of the extracts of these plants to offer protection against acute hepatotoxicity induced by paracetamol (150 mg/kg) in Swiss albino mice. Oral administration of A. paniculata or S. chirayita extract (100–200 mg/kg) offered a significant dose dependent protection against paracetamol induced hepatotoxicity as assessed in terms of biochemical and histopathological parameters. The paracetamol induced elevated levels of serum marker enzymes such as serum glutamate pyruvate transaminase (GPT), serum glutamate oxaloacetate transaminase (GOT), alkaline phosphatase (ALP), and bilirubin in peripheral blood serum and distorted hepatic tissue architecture along with increased levels of lipid peroxides (LPO) and reduction of superoxide dismutase (SOD), catalase, reduced glutathione (GSH) and glutathione peroxidase (GPx) in liver tissue. Administration of the plant extracts after paracetamol insult restored the levels of these parameters to control (untreated) levels. Thus the present study revealed that the extracts of A. paniculata or S. chirayita offered protection against hepatotoxicity induced by paracetamol.     

Influence of naringenin on oxytetracycline mediated oxidative damage in rat liver

Naringenin is a naturally occurring citrus flavanone, which has been reported to have a wide range of pharmacological properties. The present work was carried out to evaluate the effect of naringenin on antioxidant and lipid peroxidation status in liver of oxytetracycline-intoxicated rats. Intraperitonial administration of oxytetracycline 200 mg/kg for 15 days resulted a significant elevation in serum hepatospecific markers such as aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase, and bilirubin and the levels of lipid peroxidation markers (thiobarbituric acid reactive substances (TBARS) and lipid hydroperoxides) in liver. Oxytetracycline also caused a significant reduction in the activities of superoxide dismutase, catalase, glutathione peroxidase, reduced glutathione (GSH), vitamin C and vitamin E in liver. Oral administration of naringenin (50 mg/kg b.w.t.) with oxytetracycline significantly decreased the activities of serum aspartate transaminase, alanine transaminase, alkaline phosphatase, lactate dehydrogenase and the levels of bilirubin along with significant decrease in the levels of lipid peroxidation markers in the liver. In addition, naringenin significantly increased the activities of superoxide dismutase, catalase and GSH peroxidase as well as the level of GSH, vitamin C and vitamin E in liver of the oxytetracycline-treated rats. Our results demonstrate that naringenin exhibited antioxidant property and decrease the lipid peroxidation against oxytetracycline-induced oxidative stress in liver.     

Taurine treatment reduces hepatic lipids and oxidative stress in chronically ethanol-treated rats

In this study, we evaluated whether taurine treatment has a protective effect on the prooxidant-antioxidant state following chronic ethanol treatment in rats. Rats were given water containing 20% ethanol (v/v) as drinking water for 3 months. Chronic ethanol treatment in drinking water resulted in increased oxidative stress in the liver of rats. Taurine treatment was performed by adding 1% taurine (w/v) to the drinking water plus injection (400 mg/kg body weight) intraperitoneally 3 times/week for 28 d after ethanol cessation in chronically ethanol-treatad rats. This treatment starting after ethanol cessation caused a significant decreases in serum transaminase activities and hepatic total lipid, triglyceride, malondialdehyde, and diene conjugate levels and significant increases in hepatic glutathione, vitamin E, and vitamin C levels, but did not alter the activities of superoxide dismutase, glutathione peroxidase, and glutathione transferase in the liver as compared with chronically ethanol-treated rats. Accordingly, we propose that taurine has a restorative effect on ethanol-induced hepatic damage by decreasing oxidative stress.     

Potential beneficial effect of naringenin on lipid peroxidation and antioxidant status in rats with ethanol‐induced hepatotoxicity

Objectives The aim was to study the effect of naringenin, a biologically active compound, on tissue antioxidant status and lipid peroxidation in ethanol‐induced hepatotoxicity in rats. Methods Rats were divided into four groups: Groups 1 and 2 received isocaloric glucose and 0.5% carboxymethyl cellulose; groups 3 and 4 received 20% ethanol equivalent to 6 g/kg daily for 60 days. In addition, groups 2 and 4 were given naringenin (50 mg/kg) daily for the last 30 days of the experiment. Key findings The results showed significantly elevated levels of serum aspartate and alanine transaminases, γ‐glutamyl transpeptidase, tissue thiobarbituric acid reactive substances, conjugated dienes, lipid hydroperoxides and protein carbonyl content, and significantly lowered activities/levels of antioxidants such as superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase, glutathione‐S‐transferase, reduced glutathione and vitamins C and E in ethanol‐treated rats compared with control rats. Administration of naringenin to rats with ethanol‐induced liver injury significantly decreased the levels of serum aspartate and alanine transaminases, γ‐glutamyl transpeptidase, tissue thiobarbituric acid reactive substances, conjugated dienes, lipid hydroperoxides and protein carbonyl content and significantly elevated the activities of superoxide dismutase, catalase, glutathione peroxidase, glutathione reductase and glutathione‐S‐transferase, and the levels of reduced glutathione and vitamins C and E in the tissues compared with unsupplemented ethanol‐treated rats. Histological changes observed in the liver correlated with the biochemical findings. Conclusions Taken together these findings suggest that naringenin has a therapeutic potential in the abatement of ethanol‐induced hepatotoxicity.     

Nelumbo nucifera leaf extract treatment attenuated preneoplastic lesions and oxidative stress in the livers of diethylnitrosamine‐treated rats

Lotus (Nelumbo nucifera Gaertn) possesses antioxidant, hepatoprotective, and anticancer potential. This study determined the protective role of aqueous extract from Nelumbo nucifera leaves (NLE) against N‐diethylnitrosamine (DEN)‐induced oxidative stress and hepatocellular carcinogenesis in a sample of Sprague–Dawley rats. NLE was fed orally to rats in which hepatic carcinoma was induced with DEN for 12 weeks. Five groups of 12 rats each were used for the study: Group I (control group) rats received distilled water; Group II rats were induced with DEN; Group III rats were induced with DEN and cotreated with 0.5% NLE; Group IV rats were induced with DEN and cotreated with 1.0% NLE; and Group V rats were induced with DEN and cotreated with 2.0% NLE. Clinical chemistry, organ weight, inflammatory marker, protein expression, enzyme, and antioxidant analyses were conducted. NLE administration to rats resulted in significantly decreased levels of serum alanine aminotransferase, aspartate aminotransferase, and albumin, which is indicative of hepatocellular damage, compared with the control group. DEN‐induced oxidative stress was inhibited by NLE and this inhibition was paralleled by decreased lipid peroxides and increased glutathione transferase, superoxide dismutase, catalase, and glutathione peroxidase activity in liver tissues. The status of nonenzymatic antioxidants, such as reduced glutathione, was also found to be increased in NLE‐administered rats. Furthermore, NLE decreased tumor size, hepatic Rac1, PKCα, and GSTπ expressions compared with the DEN‐only group. Thus, supplementation of NLE reduced the adverse changes that occur because of liver cancer. These results prove that NLE protects against liver carcinogenesis induced because of treatment with DEN through blocking lipid peroxidation, hepatic cell damage, and enhancing the antioxidant defense system.     

Hepatic mitochondrial prooxidant and antioxidant status in ethanol-induced liver injury in rats

In this study, prooxidant and antioxidant status in liver homogenates and their mitochondrial fractions were investigated in both chronic and chronic plus acute ethanol-treated rats. Increases in serum transaminase activities, as well as increases in total lipid, triglyceride, malondialdehyde (MDA) and diene conjugate (DC) levels and decreases in glutathione (GSH), vitamin E and vitamin C levels, have been observed in liver homogenates following chronic ethanol treatment (20% ethanol, v/v as drinking water for 3 months), but CuZn-superoxide dismutase (CuZnSOD), glutathione peroxidase (GSH-Px) and glutathione transferase (GST) activities remained unchanged in postmitochondrial fractions. When an acute dose of ethanol (5 g/kg, i.p.) was given rats which had received ethanol chronically, serum transaminase activities and hepatic lipid and MDA and DC levels increased further, but GSH levels and antioxidant enzymes decreased more compared to the chronic ethanol-treated rats. There were no significant differences in the levels of MDA, DC and protein carbonyl and the activities of GSH-Px and GST in the hepatic mitochondrial fraction of rats following both chronic and chronic plus acute treatments. Mn-superoxide dismutase (MnSOD) activities increased in both groups, but mitochondrial GSH levels decreased only after chronic plus acute treatment. Therefore, we suggest that the increase in MnSOD activity may play an important role in the regulation of mitochondrial susceptibility against ethanol-induced oxidative stress.     

Silymarin modulates the oxidant-antioxidant imbalance during diethylnitrosamine induced oxidative stress in rats

Oxidative stress is a common mechanism contributing to initiation and progression of hepatic damage in a variety of liver disorders. Hence, there is a great demand for the development of agents with potent antioxidant effect. The aim of the present investigation is to evaluate the efficacy of silymarin as a hepatoprotective and an antioxidant against diethylnitrosamine induced hepatocellular damage. Single intraperitoneal administration of diethylnitrosamine (200 mg/kg) to rats resulted in significantly elevated levels of serum aspartate transaminase (AST) and alanine transaminase (ALT), which is indicative of hepatocellular damage. Diethylnitrosamine induced oxidative stress was confirmed by elevated levels of lipid peroxidation and decreased levels of superoxide dismutase (SOD), catalase, glutathione peroxidase, glutathione reductase (GR) and glutathione-S-transferase (GST) in the liver tissue. The status of non-enzymic antioxidants like, vitamin-C, vitamin-E and reduced glutathione (GSH) were also found to be decreased in diethylnitrosamine administered rats. Further, the status of membrane bound ATPases was also altered indicating hepatocellular membrane damage. Posttreatment with the silymarin (50 mg/kg) orally for 30 days significantly reversed the diethylnitrosamine induced alterations in the liver tissue and offered almost complete protection. The results from the present study indicate that silymarin exhibits good hepatoprotective and antioxidant potential against diethylnitrosamine induced hepatocellular damage in rats.     

Hepatoprotective activity of Amaranthus spinosus in experimental animals

The hepatoprotective and antioxidant activity of 50% ethanolic extract of whole plant of Amaranthus spinosus (ASE) was evaluated against carbon tetrachloride (CCl₄) induced hepatic damage in rats. The ASE at dose of 100, 200 and 400 mg/kg were administered orally once daily for fourteen days. The substantially elevated serum enzymatic levels of serum glutamate oxaloacetate transaminase (AST), serum glutamate pyruvate transaminase (ALT), serum alkaline phosphatase (SALP) and total bilirubin were restored towards normalization significantly by the ASE in a dose dependent manner. Higher dose exhibited significant hepatoprotective activity against carbon tetrachloride induced hepatotoxicity in rats. The biochemical observations were supplemented with histopathological examination of rat liver sections. Meanwhile, in vivo antioxidant activities as malondialdehyde (MDA), hydroperoxides, reduced glutathione (GSH), superoxide dismutase (SOD) and catalase (CAT) were also screened which were also found significantly positive in a dose dependent manner. The results of this study strongly indicate that whole plants of A. spinosus have potent hepatoprotective activity against carbon tetrachloride induced hepatic damage in experimental animals. This study suggests that possible mechanism of this activity may be due to the presence of flavonoids and phenolics compound in the ASE which may be responsible to hepatoprotective activity.     

Effect of ethanol extract of Embelia ribes fruits on cardiac changes in rats subjected to ischemic reperfusion injury

The present study evaluated the cardioprotective potential of ethanol extract of Embelia ribes Burm. (Myrsinaceae) fruits on left anterior descending coronary artery ligation (LAD)-induced myocardial infarction in albino rats. In open-chest chloral hydrate (400?mg/kg, i.p.) anesthetized rats, the left anterior descending coronary artery was occluded for 30?min followed by 90?min of reperfusion. Vehicle (1% Tween 80 in distilled water) or ethanol Embelia ribes extract (100 and 200?mg/kg, orally) was administered for 7 days (pre-treatment). In the vehicle-treated group, ischemic-reperfusion injury (IRI) was evidenced by depression of hemodynamic function (heart rate), raised levels of serum lactate dehydrogenase (LDH) and myocardial thiobarbituric acid reactive substances (TBARS) levels and depletion of endogenous myocardial antioxidants (glutathione (GSH), glutathione peroxidase (GPx), glutathione reductase (GR) and glutathione-S-transferase (GST)) and Na-K-ATPase levels, as compared to sham rats. Pre-treatment with ethanol Embelia ribes extract prevented 1) loss of myocardial hemodynamic function, 2) rise in serum LDH and myocardial TBARS levels, and 3) depletion of myocardial endogenous antioxidants and Na-K-ATPase levels. The results of the present study, suggests that ethanol Embelia ribes extract treatment enhances the antioxidant defense against LAD-induced ischemic-reperfusion injury in rats and exhibits cardioprotective property.     

Effects of diallyl tetrasulfide on cadmium-induced oxidative damage in the liver of rats

The protective efficacy of diallyl tetrasulfide (DTS) from garlic on liver injury induced by cadmium (Cd) was investigated. In this study, Cd (3 mg/kg body weight) was administered subcutaneously for 3 weeks to induce toxicity. DTS was administered orally (10, 20 and 40 mg/kg body weight) for 3 weeks with subcutaneous (sc) injection of Cd. Cd-induced liver damage was evidenced from increased activities of serum hepatic enzymes, namely aspartate transaminase, alanine transaminase, alkaline phosphatase and lactate dehydrogenase, with significant elevation of lipid peroxidation indices (thiobarbituric acid reactive substances and hydroperoxides) and protein carbonyl groups in the liver. Rats subjected to Cd toxicity also showed a decline in the levels of total thiols, reduced glutathione (GSH), vitamin C and vitamin E, accompanied by an increased accumulation of Cd, and significantly decreased activities of superoxide dismutase, catalase (CAT), glutathione peroxidase, glutathione-S-transferase (GST), glutathione reductase, and glucose-6-phosphate dehydrogenase in the liver. Administration of DTS at 40 mg/kg body weight significantly normalised the activities of hepatic marker enzymes, compared to other doses of DTS (10 and 20 mg/kg body weight). In addition, DTS (40 mg/kg body weight) significantly reduced the accumulation of Cd and the level of lipid peroxidation, and restored the level of antioxidant defense in the liver. Histological studies also showed that administration of DTS to Cd-treated rats resulted in a marked improvement of hepatocytes morphology with mild portal inflammation. Our results suggest that DTS might play a vital role in protecting Cd-induced oxidative damage in the liver.     

The effects of fucoidan extracts on CCl<Subscript>4</Subscript>-induced liver injury

The aim of this study was to elucidate the antioxidant properties of fucoidan extracts (FE) against CCl(4)-induced oxidative stress by monitoring the levels of glutamate oxaloacetate transaminase (GOT), glutamate pyruvate transaminase (GPT), alkaline phosphatase (ALP), lactate dehydrogenase (LDH), malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT) and glutathione peroxidase (GPx). Female, Sparague-Dowley rats were administered with FE (100 mg/kg daily) for 14 days and CCl(4) on the 15'th day, 12 h before they were sacrificed. The levels of GOT, GPT, ALP and LDH in serum of rats, as well as the levels of MDA, SOD, CAT and GPx in total liver homogenate were analyzed. CCl(4)-treatment was found to increase the levels of GOT, GPT, ALP, LDH and MDA, as well as decrease levels of SOD, CAT and GPx significantly. The pre-treatment of rats with FE, however, suppressed the increment of levels of GOT, GPT, ALP, LDH and MDA, as well as recovered the levels of SOD, CAT and GPx in CCl(4)-treated rats. Moreover there was a significant decrease in incidences of necrosis and cirrhosis in the liver tissue of FE-treated rats. These results implied that FE possessed antioxidant properties against CCl(4)-induced oxidative stress.     

The protective effect of taurine against thioacetamide hepatotoxicity of rats

Thioacetamide (TAA) administration (three consecutive intraperitoneal injections of 400 mg/kg at 24-h interval) to rats resulted in hepatic injury as assessed by the measurement of serum transaminase activities and histopathological findings. This treatment caused an increase in the levels of malondialdehyde (MDA), diene conjugates (DCs) and glutathione (GSH) and the activity of superoxide dismutase SOD ), and a decrease in the levels of vitamins E and C and the activity of glutathione peroxidase (GSH-Px) in the liver of rats. Taurine administration (400 mg/kg, i.p., every 12 h and started 24 h prior to the first TAA injection) was found to decrease serum transaminase activities and hepatic lipid peroxidation without any significant change in hepatic antioxidant system. Histopathological findings also suggested that taurine has ameliorated effect on TAA-induced hepatic necrosis. These results indicate that taurine treatment, together with TAA administration, diminished the severity of the liver injury by decreasing oxidative stress due to its possible scavenger effect.     

Hypoglycaemic effect of Melothria heterophylla in streptozotocin-induced diabetic rats

Context: In the Indian traditional system of medicine, Melothria heterophylla (Lour.) Cogn., (Cucurbitaceae) is prescribed for the treatment of diabetes mellitus. Objective: In the present study, the antidiabetic effect of ethanol extract of Melothria heterophylla (EEMH), and its active isolated constituents were investigated in streptozotocin (STZ)-induced diabetic Swiss albino rats. Method: Successive Soxhlet extraction of the dried total aerial parts with petroleum ether for defatting and then with ethanol (95%) to obtain ethanol extract, which was concentrated under reduced pressure. Hyperglycemia was induced in rats by STZ (50 mg/kg, body weight). Twenty-four hours after STZ induction, respective groups of diabetic rats received EEMH (200 and 400 mg/kg, body weight), gallic acid (GA) (2 and 4 mg/kg, body weight), and rutin (RU) (2 and 4 mg/kg, body weight), respectively, orally daily for 15 days. Glibenclamide (0.5 mg/kg, orally) served as reference. Blood glucose levels and change in body weight were measured on every 5(th) day during 15 days of treatment. Biochemical parameters, viz., serum glutamic oxaloacetic transaminase (SGOT), serum glutamic pyruvic transaminase (SGPT), alkaline phosphatase (ALP) and serum insulin, were measured. Results: EEMH and its active constituents significantly (p < 0.01) normalized blood glucose levels and serum biochemical parameters as compared to those of STZ controls. Both GA (4 mg/kg) and RU (4 mg/kg) exhibited maximum glucose lowering effect (69.1 and 66.7%, respectively) in diabetic rats compared to the other dose (2 mg/kg) at the end of the study. EEMH, gallic acid and RU also showed significant increase in serum insulin, and body weight of STZ-induced diabetic rats. Conclusion: Therefore, ethanol extract of Melothria heterophylla, GA and RU demonstrated remarkable antidiabetic activity in STZ-induced diabetic rats.