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

Hesperetin is the main pharmacological ingredient of fruit of the citrus family, rutaceae. It is a flavanone, 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-[alpha]), interleukin (IL)-1[beta], 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-[gamma] (PPAR-[gamma]). 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-[alpha], IL-1[beta], 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-[gamma] (PPAR-[gamma]) 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-[gamma] and Bcl-2 in the model mice. Key words: hesperidin, acute myocardial infarction, peroxisome proliferator-activated receptor-[gamma], B-cell lymphoma 2