Molecular Mechanisms Underlying the Protective Effect of Telmisartan in Non-Alcoholic Fatty Liver Disease: Role of Proinflammatory Enzymes

Background: Non-alcoholic fatty liver disease (NAFLD) is an increasingly recognized condition that may progress to end stage liver cell failure. There is as yet no clearly established therapy for prevention or treatment of NAFLD. Telmisartan, an angiotensin II receptor blockers and partial agonist on peroxisome proliferative activated receptor-gamma (PPAR-γ), showed a promising protective effect in NAFLD. Aim: The present study explored the mechanism(s) of the protective effect of telmisartan on NAFLD with a focus on the role of the proinflammatory enzymes: induced nitric oxide synthase (iNOS) and cyclooxygenase-2 (COX-2). Methods: Adult male Wistar rats were assigned into three groups and treated for 8 weeks as follow: group 1 fed normal diet and served as normal control group; group 2 fed high cholesterol diet; group 3 fed high cholesterol diet plus telmisartan. Results: Administration of telmisartan in cholesterol-fed rats attenuated the development of NAFLD as evidenced by significant decrease in liver index and confirmed by histopathological examination. The effect of telmisartan was accompanied with significant decrease in hepatic tissue expression of the proinflammatory enzymes: iNOS and COX-2. Conclusion: Telmisartan inhibited the proinflammatory mediators, iNOS and COX-2, reported to be involved in the progression of NAFLD indicating that telmisartan might serve as a potential therapy for NAFLD.