Preventive effect of hesperidin modulates inflammatory responses and antioxidant status following acute myocardial infarction through the expression of PPAR-γ and Bcl-2 in model mice

Abstract

Hesperetin is the main pharmacological ingredient of fruit of the citrus family, rutaceae. It is a fiavanone, which has potent antioxidation and anti-inflammatory activities. The present study investigated the preventive effect of hesperidin in the modulation of acute myocardial infarction (AMI)-induced inflammatory responses and antioxidant status in a mouse model. The levels of creatine kinase-MB, tumor necrosis factor (TNF-α), interleukin (IL)-1β, IL-6, monocyte chemoattractant protein 1 (MCP-1), intercellular adhesion molecule 1 (ICAM-1), malondialdehyde (MDA), catalase (CAT), superoxide dismutase (SOD) and caspase-3/9 were measured using ELISA kits. Western blot analysis analyzed p53 and B-cell lymphoma 2 (Bcl-2)-associated X protein/Bcl-2, and induced the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ). Hesperidin markedly decreased the myocardial infarction area, heart weight/body weight ratio and activity of creatine kinase-MB in AMI mice. Hesperidin treatment caused a significant decrease in the levels of TNF-a, IL-lp, IL-6, MCP-1, ICAM-1, MDA, CAT, SOD and caspase-3/9 in mice with AMI. Hesperidin also significantly suppressed the protein expression levels of p53 and Bax/Bcl-2, and induced the expression of peroxisome proliferator-activated receptor-γ (PPAR-γ) in mice with AMI. The preventive effect of hesperidin modulated the inflammatory response and antioxidant status following AMI through downregulation of the expression of PPAR-γ and Bcl-2 in the model mice.