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HD-03对实验性肝硬化的抑制
AIM: To investigate the protective effect of HD-03 in experimental cirrhosis following chronic intoxication with thioacetamide ( TAA ). METHODS: The effect of HD-03 (750 mg/kg po ) was studied in rats following TAA-induced intoxication (50 mg/kg po ) for a period of 90 d. HD-03 was administered as an aqueous suspension. Levels of biochemical markers indicative of hepatotoxicity were assessed in serum and liver. Histopathological evaluation of liver was also carried out to find out the protective effect of HD-03 following TAA-induced chronic intoxication. RESULTS: Administxation of TAA at a dose of 50 mg/kg po for 90 d resulted in a significant derangement of serum [ serum glutamic pyruvate transaminase (SGPT), serum glutamic oxaloacetate transaminase (SGOT), alkaline phosphatase (ALP), albumin and bilirubin ] and hepatic ( triglycerides, protein, hydroxyproline, collagen and glycogen) biochemical parameters. Histopathological evaluation of liver sections following TAA-intoxication showed necrosis and proliferative changes characteristic of cirrhosis. Simultaneous treatment of TAA-intoxicated rats with HD-03 at a dose of 750 mg/kg po for the same duration significantly prevented the changes in both serum and hepatic biochemical parameters. The reversal of serum and hepatic biochemical parameters also correlated with the preservation of liver histoarchitecture in HD-03 treated rats. CONCLUSION: The responses such as membrane stabilization,hepatocellular regeneration, and inhibition of collagen formation are the contributing factors in the correction of TAA-induced cirrhosis by HD-03.
