Possible effects of interferon-alpha on Fas-induced renal apoptosis in mouse

Abstract

Fas (APO-1/CD95) is a cell surface receptor that initiates apoptotic pathway. Fas-stimulated ROS generation may play important role in Fas-mediated apoptosis. The aim of this study was to evaluate the influence of interferon-alpha on oxidative stress parameters in Fas-induced renal apoptosis in mice kidney.

Subjects and methods: One-month-old Balb C male mice were used for the study. The animals were divided in four groups: group 1 were the controls, group 2 mice were treated with anti-Fas antibody i.p., group 3 mice were treated with IFN-alpha, and group 4 mice were treated with both agents simultaneously. The mice were killed 48 h afterwards, and kidneys were homogenized. TBA reactive substances (TBARS), glutathione content, and reactive carbonyl group (RCG) were measured.

Results: The results showed a statistically significant increase of TBARS (p < 0.05) and RCG (p < 0.05) concentration in the group treated with anti-Fas antibody versus control. IFN-alpha decreased the concentration of TBARS and RCG after anti-Fas antibody administration (p < 0.05). There is no significant difference in glutathione content between investigated groups.

Conclusion: IFN-alpha might be considered as a new target for therapeutic intervention in FasL/Fas induced renal injury.