Fenugreek seeds attenuate thioacetamide induced liver damage.

The intention to conduct this study was to evaluate the hepatoprotective effects of Fenugreek seeds' extract supplementation in thioacetamide induced liver damage in male Sprague Dawley rats. For this study, 24 male Sprague Dawley rats (200-264gm) were distributed randomly into four groups. Group I remained untreated as control rats, group II received thioacetamide (200mg/Kg b.w i.p, administered on alternative days for 8 weeks), group III received thioacetamide (200mg/Kg b.w i.p administered on alternative days for 8 weeks) as well as 2ml of 2% extract of fenugreek seeds (orally administered daily from 4th week till 8th week of the experiment. Group IV only received 2ml of 2% extract of Fenugreek seeds daily for 4 weeks respectively. At the end of the experiment, blood was sampled to obtain plasma that was used for the analysis of liver markers and liver was used for analysis of antioxidant enzymes (catalase and SOD). Increase in total bilirubin, direct bilirubin, ALT and ALP levels, catalase activity and decrease in SOD activity was found in TAA-treated groups which assured liver damage. Whereas, treatment with Fenugreek seeds extract restored the altered levels of total bilirubin, direct bilirubin, ALT, ALP, catalase and SOD activities in the Test + Supp group. The results of this study confirmed the hepatoprotective role of Fenugreek seeds extract in thioacetamide induced liver damage.

Effect of salicylic acid supplementation on blood glucose, lipid profile and electrolyte homeostasis in gentamicin sulphate induced nephrotoxicity.

This study was designed to investigate effect of salicylic acid supplementation in gentamicin- induced nephrotoxicity. For this purpose, twenty four male albino rabbits were divided into 4 groups (n=6); control group, healthy untreated rabbits; gentamicin group, received only gentamicin (80mg/kg); gentamicin + salicylic acid group, received gentamicin (80mg/kg) + salicylic acid (80mg/kg) and salicylic acid group, received only salicylic acid (80mg/kg) through intra peritoneal route for 21 consecutive days. Biochemical evaluation was carried out by assessment of body weights and by estimating plasma glucose, lipid profile and electrolyte homeostasis. Gentamicin sulphate induction resulted in increased plasma glucose, plasma TG, plasma cholesterol, plasma LDL, and plasma sodium and in decreased plasma HDL and plasma potassium with significant reduction in body weights in GS-treated group, which were restored by supplementation with salicylic acid in GS+SA treated group. Therefore, these findings confirm the protective role of salicylic acid in gentamicin- induced nephrotoxicity in rabbits.

Nephroprotective effects of b-carotene on ACE gene expression, oxidative stress and antioxidant status in thioacetamide induced renal toxicity in rats.

ß -carotene is one of carotenoid natural pigments, which are produced by plants and are accountable for the bright colors of various fruits and vegetables. These pigments have been widely studied for their ability to prevent chronic diseases and toxicities. This study was designed to evaluate the effects of ß-carotene on angiotensin converting enzyme (ACE) gene expression, oxidative stress and antioxidant status in thioacetamide induced renal toxicity. Total 24 albino wistar rats of male sex (200-250gm) were divided into 6 groups as Group-1: The control remained untreated; Group-2: Received thioacetamide (200mg/kg b.w; i.p) for 12 weeks; Group-3: Received ß-carotene orally (200mg/kg b.w), for 24 weeks; and Group-4: Received thioacetamide (200mg/kg b.w; i.p) for 12 weeks + received ß-carotene orally (200mg/kg b.w), for further 12 weeks. The expression of ACE gene in thioacetamide induced renal toxicity in rats as well as supplemented with ß-carotene was investigated and compared their level with control groups by using the quantitative RT-PCR method. The ACE gene expression was significantly increase in TAA rats as compare to control rats specifies that TAA induced changes in ACE gene of kidney, elevated renal ACE has been correlated with increase hypertensive end organ renal damage. The quantity of ACE gene were diminish in our rats who received ß-Carotene after TAA is administered, for this reason they seemed to be defended against increased ACE levels in kidney bought by TAA. In pre- and post-treatment groups, we studied the role of ß-Carotene against thioacetamide in the kidney of Wistar rats. Experimental confirmation from our study illustrates that ß-Carotene can certainly work as a successful radical-trapping antioxidant our results proved that TAA injury increased lipid peroxidation and diminish antioxidant GSH, SOD and CAT in renal tissue. Since ß-Carotene administration recover renal lipid peroxidation and antioxidants, it give the impression that ß-Carotene protects renal tissue against thioacetamide-induced oxidative damage.

Effects of curcumin on angiotensin-converting enzyme gene expression, oxidative stress and anti-oxidant status in thioacetamide-induced hepatotoxicity.

INTRODUCTION: This study aimed to evaluate the protective effects of curcumin on angiotensin-converting enzyme (ACE) gene expression, oxidative stress and anti-oxidant status in thioacetamide (TAA)-induced hepatotoxicity in rats. MATERIALS AND METHODS: Total 32 albino Wistar rats (male, 200-250 g) were divided into six groups (n=8). Group 1: untreated controls; Group 2: received TAA (200 mg/kg body weight (b.w.); i.p.) for 12 weeks; Group 3: received curcumin (75 mg/kg b.w.) for 24 weeks; Group 4: received TAA (200 mg/kg b.w.; i.p.) for 12 weeks+curcumin (75 mg/kg b.w.) for 12 weeks. RESULTS: A significantly higher ACE gene expression was observed in TAA-induced groups as compared with control, indicating more synthesis of ACE proteins. Treatment with curcumin suppressed ACE expression in TAA liver and reversed the toxicity produced. TAA treatment results in higher lipid peroxidation and lower GSH, SOD and CAT than the normal, and this produces oxidative stress in the liver. Cirrhotic conditions were confirmed by serum enzymes (ALT, AST and ALP) as well as histopathological observations. CONCLUSION: Curcumin treatment reduced oxidative stress in animals by scavenging reactive oxygen species, protecting the anti-oxidant enzymes from being denatured and reducing the oxidative stress marker lipid peroxidation. Curcumin treatment restores hepatocytes, damaged by TAA, and protects liver tissue approaching cirrhosis.

Role of selenium in protection of liver cirrhosis.

Selenium is an essential trace element and has been shown to protect the rats against dietary liver necrosis. This study was designed to evaluate the effects of selenium supplementation on different biochemical parameters in thioacetamide induced cirrhotic rats. For this purpose 24 male Albino wistar rats were divided into four groups (n=6). Group I, remained healthy control rats, Group II, received thioacetamide (at a dose of 200mg/kg b.w, i.p, for 12 weeks, twice a week) in first phase and saline in second phase, Group III, received thioacetamide (200mg/kg b.w, i.p for 12 weeks, twice a week) in first phase and sodium selenite ((1mg/kg b.w, i.p. for 12 weeks, three times a week ) in second phase and Group IV, received sodium selenite (1mg/kg b.w, i.p. for 12 weeks, three times a week) in first phase and saline in second phase. Biochemical analysis was evaluated by total and direct bilirubin, liver specific enzymes, and antioxidant enzymes. Marked increase in total and direct bilirubin and ALT activity was the indicative markers of liver cirrhosis while reduced antioxidant activity (SOD and GSH) and increased MDA and Catalase levels were observed in cirrhotic group. Sodium selenite supplementation markedly reduced total bilirubin and ALT activity and restored the antioxidant enzymes (SOD and GSH) and MDA and catalase activity. These results indicate that sodium selenite successively attenuates the thioacetamide induced liver cirrhosis.

Angiotensin converting enzyme (ACE) gene expression in experimentally induced liver cirrhosis in rats.

Angiotensin converting enzyme (ACE) is a key player of Renin Angiotensin System (RAS), involved in conversion of active product, angiotensin-II. Alterations in RAS have been implicated in the pathophysiology of various diseases involving heart, kidney, lung and liver. This study is designed to investigate the association of ACE gene expression in induction of liver cirrhosis in rats. Total 12 male albino Wistar rats were selected and divided in two groups. Control group received 0.9% NaCl, where as Test group received thioacidamide (TAA), dissolved in 0.9%NaCl, injected intraperitoneally at a dosage of 200mg/Kg of body weight, twice a week for 12 weeks. The rats were decapitated and blood sample was collected at the end of experimental period and used for liver functions, enzyme activity, antioxidant enzymes and lipid peroxidation estimations. Genomic DNA was isolated from excised tissue determine the ACE genotypes using specific primers. The ACE gene expression in liver tissue was assessed using the quantitative RT-PCR method. The activity of ALT, total and direct bilirubin, SOD and CAT levels were significantly high (p<0.05) and level of MDA was significantly low (p<0.05) in TAA treated rats as compared to control rats. The ACE gene expression after 12 weeks TAA treatment in cirrhotic rats was significantly increased (p<0.05) in comparison to controls. This study describes the importance of RAS in the development of hepatic fibrosis and the benefits of modulation of this system ACE gene expression. The finding of major up-regulation of ACE in the experimental rat liver provides further insight into the complexities of the RAS and its regulation in liver injury. The development of specific modulators of ACE activity and function, in future, will help determine the role of ACE and its genetic variants in the pathophysiology of liver disease.