Does telmisartan prevent hepatic fibrosis in rats with alloxan-induced diabetes?

HALICI Z., Bilen H., ALBAYRAK F., UYANIK A., Cetinkaya R., Suleyman H., ...More

European Journal of Pharmacology, vol.614, no.1-3, pp.146-152, 2009 (SCI-Expanded) identifier identifier

  • Publication Type: Article / Article
  • Volume: 614 Issue: 1-3
  • Publication Date: 2009
  • Doi Number: 10.1016/j.ejphar.2009.04.042
  • Journal Name: European Journal of Pharmacology
  • Journal Indexes: Science Citation Index Expanded (SCI-EXPANDED), Scopus
  • Page Numbers: pp.146-152
  • Keywords: Angiotensin, Diabetes mellitus, Liver, Stereology, TGF-β
  • Erzincan Binali Yildirim University Affiliated: No


Background/aims: This study evaluated the effect of telmisartan on the livers of diabetic rats and also aimed to determine the hepatic distribution and role of transforming growth factor β (TGF-β) in diabetes-related hepatic degeneration while taking into account the possible protective effects of telmisartan. Methods: Fifteen adult male rats were used and divided into three groups: the non-diabetic healthy group, alloxan-induced diabetic control group, and the alloxan-induced diabetic telmisartan group. The non-diabetic healthy group and the diabetic control group were exposed to saline for 30 days, while the group treated with diabetic drugs was orally administered telmisartan for 30 days (10 mg/kg/day). At the end of the experiment, the rats were sacrificed and the livers were dissected and transferred into the fixation solution. The livers were then evaluated using stereological and histopathological methods. Results: Our study of the numerical density of hepatocytes shows a significant difference between the diabetic control group and diabetic rats treated with telmisartan. Immunohistochemical staining for TGF-β in liver sections of the diabetic rats treated with telmisartan showed no immunoreactivity. The diabetic control group was determined to be strongly immunoreactive to TGF-β. Conclusion: Results suggest that telmisartan may reduce type-I diabetes mellitus-induced hepatic injury by suppressing activated hepatic stellate cells through concomitant TGF-β1 down-regulation. © 2009 Elsevier B.V. All rights reserved.