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.

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‑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‑α, IL‑1β, 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.