effect of different doses of silymarin on gentamicin-induced kidney damage in rats

Many in vivo and in vitro studies performed mainly in liver have been shown silymarin to be a potent anti-oxidant, and one of the most potent scavengers of hydroxyl radicals. Therefore, it is plausible to expect that it may produce these effects against oxidalive stress consequences induced by gentamicin in the kidney. Evaluation of the protective effect of different doses of silymarin given orally in protecting rats against gentamicin-induced nephrotoxicity. Groups of rats [6 rats each] were pre-treated for 7 days with 250, 500, and l000 mg/kg silymarin and vehicle orally before induction of renal toxicity with gentamicin, and another 6 rats were utilized as controls. The parameters of oxidative stress, malondialdehyde [MDA], and glutathione [GSH] were measured in the serum and kidney tissue homogenate, in addition to serum levels of urea and creatinine. Histopathological examination of stained tissue sections from the kidney was performed; in addition to silymarin level in the kidney tissue homogenate was evaluated using HPLC method. Analysis of data revealed significant amelioration of oxidative stress, experimentally induced in the kidney through lowering MDA and elevation of GSH levels, both in serum and tissue homogenate, associated with significant reduction of serum levels of urea and creatinine, and with positive histological evidences for the protective effect of silymarin which is found to be related to the increase in its renal tissue availability when the oral dose was increased. These findings suggest that, silymarin is effective in preventing gentamicin-induced renal toxicity, which makes it a good candidate for clinical use in this respect

Dose-dependent protective effects of silymarin against ccu-induced liver damage in rats

Silymarin, the dried extract of the ripe seeds of Silybum marianum is found to be a powerful protective agent against xenobiotics-induced tissue injury in many organs, including liver. However, the dose-dependent relationship of this effect and tissue availability is not fully explored. So, this project was designed to evaluate the relationship between dose, tissue availability and tissue protection of silymarin against ccu-induced hepatic toxicity in rats. The tissue protective effects of silymarin were studied through the pre-treatment of rats with various doses [250, 500, and l000 mg/kg] orally twice daily before the induction of hepatotoxicity of ccl4. Malondialdehyde [MDA] and glutathione [GSH] were evaluated in the serum and tissue homogenate. The activities of different enzymes, which are considered as indicators of organ toxicity like alanine amino transaminase [ALT] and aspartate aminotransaminase [AST] were assessed. Histopathological examination of stained tissue sections from the liver were done to evaluate the protective effect at the microscopical levels. In addition, silymarin level in liver tissue homogenate -was evaluated using HPLC method. The data obtained indicated that, a significant amelioration of oxidative stress experimentally induced in the liver of rats was produced by silymarin, as evidenced by lowering MDA contents and elevation of GSH levels both in the tissues and serum compared with controls. Serum activities of ALT and AST were normalized. Additionally, histologically evident damage in the liver had improved In addition, increasing silymarin dose after oral administration resulted in increased tissue availability of many constituents. There is a dose-dependent relationship in the hepatoprotective effect of silymarin against ccU-induced hepatotoxicity in rats