Inhibition of experimental cirrhosis in rats by HD-03

AIM: To investigate the protective effect of HD-03 in experimental cirrhosi s following chronic intoxication with thioacetamide (TAA). METHODS: The eff ect of HD-03 (750 mg/kg po) was studied in rats following TAA-induced intox ication (50 mg/kg po) for a period of 90 d. HD-03 was administered as an aq ueous suspension. Levels of biochemical markers indicative of hepatotoxicit y were assessed in serum and liver. Histopathological evaluation of liver w as also carried out to find out the protective effect of HD-03 following TA A-induced chronic intoxication. RESULTS: Administration 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 transam inase (SGOT), alkaline phosphatase (ALP), albumin and bilirubin] and hepati c (triglycerides, protein, hydroxyproline, collagen and glycogen) biochemic al parameters. Histopathological evaluation of liver sections following TAA -intoxication showed necrosis and proliferative changes characteristic of c irrhosis. Simultaneous treatment of TAA-intoxicated rats with HD-03 at a do se of 750 mg/kg po for the same duration significantly prevented the change s in both serum and hepatic biochemical parameters. The reversal of serum a nd hepatic biochemical parameters also correlated with the preservation of liver histoarchitecture in HD-03 treated rats. CONCLUSION: The responses su ch as membrane stabilization, hepatocellular regeneration, and inhibition o f collagen formation are the contributing factors in the correction of TAA- induced cirrhosis by HD-03.