Olmesartan significantly attenuated increases in aspartate aminotransferase, activation of hepatic stellate cells, oxidative stress, and liver fibrosis in a rat model of nonalcoholic steatohepatitis.
Does olmesartan reduce biochemical, histologic, and antioxidant measures of disease activity in a rat model of nonalcoholic steatohepatitis?
In a rat model of NASH, the ARB olmesartan significantly reduced hepatic fibrosis, oxidative stress, and stellate cell activation, suggesting a potential therapeutic role.
UNLABELLED: Nonalcoholic steatohepatitis (NASH) is now the most frequent cause of chronic liver impairment in developed countries and is a suggested causative factor in the development of cryptogenic cirrhosis and hepatocellular carcinoma. At present there is no effective and accepted therapy for NASH. The renin-angiotensin system is involved in hepatic fibrosis through activation of hepatic stellate cells, major fibrogenic cells in the liver. Hepatic stellate cells are activated by liver injury to express excessive matrix proteins and profibrogenic cytokines such as transforming growth factor-beta 1. Medicines that inhibit this pathway may be of therapeutic potential in NASH. Using a methionine-choline-deficient rat model of NASH, we studied the potential utility of an angiotensin II type 1 receptor blocker (ARB), olmesartan, on biochemical, histologic, and antioxidant measures of disease activity. ARB significantly attenuated increases in aspartate aminotransferase, activation of hepatic stellate cells, oxidative stress, expression of transforming growth factor-beta 1, expression of collagen genes, and liver fibrosis. CONCLUSION: Our observations strongly suggest a potential preventive role for ARB in the progression of nonalcoholic steatohepatitis.
Hirose et al. (Thu,) conducted a other in Nonalcoholic steatohepatitis (NASH). Olmesartan (angiotensin II type 1 receptor blocker) was evaluated on Biochemical, histologic, and antioxidant measures of disease activity. Olmesartan significantly attenuated increases in aspartate aminotransferase, activation of hepatic stellate cells, oxidative stress, and liver fibrosis in a rat model of nonalcoholic steatohepatitis.