| Objective: To explore the protective effect of Dalbergin (DAL) on myocardial ischemia/reperfusion (MI/R) injury in mice and its mechanism. Methods: Adult male C57 BL/6J mice were randomly divided into sham operation group, model group, diltiazem group, DAL low, medium, and high dose groups (10, 30, 90 mg/kg/d), with 10 mice in each group. The mouse left anterior descending coronary artery (LAD) was ligated, ischemia for 30 minutes, and reperfusion for 1 hour to establish a mouse MI/R injury model. From the first day after the operation, mice in the sham operation group and model group were intragastrically administered with equal volume of normal saline, and mice in each dose group of DAL were intragastrically administered with the corresponding liquid once a day for 7 consecutive days. After the administration, the creatine kinase isoenzyme (CK-MB), lactate dehydrogenase (LDH) activity, tumor necrosis factor-α (TNF-α) and interleukin-6 (IL-6) in the serum of mice were detected ) Content; detection of superoxide dismutase (SOD) activity and malondialdehyde (MDA) content in mouse myocardial tissue; hematoxylin-eosin staining (HE) detection of myocardial injury pathology; Western Blot detection of Akt and P in myocardial tissue -Akt protein level expression changes; ultrasound detection of left ventricular end diastolic diameter (ESD), left ventricular end diastolic volume (EDV), ejection fraction (EF) and short axis shortening rate (FS). Results: DAL can reduce the activity of CK-MB and LDH and the content of TNF-α and IL-6 in the serum of mice; increase the activity of SOD in mouse myocardial tissue and reduce the production of MDA (P <0.01 or P <0.05); increase the expression of p-Akt protein, reduce pathological damage of myocardial tissue, and improve cardiac function. Conclusions: DAL can promote the survival of cardiomyocytes by increasing Akt phosphorylation, thereby inhibiting myocardial ischemia/reperfusion injury, and finally play a role in myocardial protection. |
