Effects of Silimarin and Curcumin against LPS-Induced Hepatotoxicity in Rats

Abstract

Hepatotoxicity is now receiving a supreme importance. LPS is the most potent activator of macrophages. The aim of this study is to demonstrate the prophylactic activity of silimarin and curcumin against LPS-induced hepatotoxicity in rats. The liver slices had been divided into 4 groups; normal, control (LPS), LPS+silimarin and LPS+curcumin (N=12). After 24 hours, analysis of NO levels, LDH activity, AST levels, ALT levels, GSH levels, TNF-α, IL-1β and IL-10 levels were carried out. . Nitric Oxide in the control group showed a high significant elevation in comparison to the normal group, while group 3 and 4 showed a high significant decrease compared with the control group. LDH activity in the control group showed a high significant elevation in comparison to the normal group, while group 3 and 4 showed a high significant decrease compared with the control group. AST and ALT in the control group showed a high significant elevation in comparison to the normal group, while group 3 and 4 showed a high significant decrease compared with the control group. In control group a significant reduction in GSH level was observed; where in group 3 and 4 a significant increase was noticed in comparison to the control group. Control group showed a high significant elevation in TNF-𝛂 level in comparison to normal group, where in group 3 and 4 a high significant decrease was detected in comparison to the control group. Levels of IL-1β in the control group indicated a high significant elevation compared to the normal group, while in group 3 and 4 a high significant decrease in the IL-1β levels were detected in comparison to the control group. IL-10 levels in the control group indicated a high significant elevation compared to the normal group, while in group 3 and 4 a high significant decrease in the IL-10 levels were detected in comparison to the control group. In conclusion, silimarin and curcumin showed a hepatoprotective activity against hepatotoxicity induced by LPS.