Canagliflozin Alleviates Apoptosis and Inflammation After Myocardial Infarction and Improves Prognosis
Objective To investigate the effect of canagliflozin(CANA)on cardiac inflammatory response and apoptosis after myocardial infarction(MI).Methods This study selected 15 C57/BL6 mice(SPF grade)aged 8~10 weeks,and randomly selected 5 mice as the Sham group(sham surgery+saline gavage)using a lottery method.The remaining 10 mice were used to create an MI model by ligating the anterior descending branch of the left coronary artery.After successful production,the 10 MI mice were randomly divided into two groups:the MI group(saline gavage)and the CANA+MI group(Canagliflozin gavage),with 5 mice in each group.The mice in the CANA+MI group were gavaged with 20 mg/(kg·d-1)of Canagliflozin for 4 weeks,while the Sham and MI groups were gavaged with the same volume of physiological saline for 4 weeks.After 4 weeks,left ventricular end systolic diameter and left ventricular ejection fraction were measured using a mouse ultrasound machine.Hematoxylin(HE staining)and Tunel staining are used to clarify the cardiac structure and cell apoptosis status after MI.IF immunofluorescence staining is used to detect the degree of cardiac inflammatory response after MI.Western blotting is used to detect the expression levels of inflammation and apoptosis related proteins.Results Compared with the MI group,left ventricular ejection fraction increased and infarct size decreased in CANA+MI group.Tunel staining showed that the number of apoptotic cells in the MI margin area of the CANA+MI group mice was significantly reduced compared to the MI group,with a corresponding decrease in the expression of pro apoptotic protein Bax and an increase in the expression of anti apoptotic protein Bcl-2.The number of CD3+T cells,F480+macrophages,and LY6G+neutrophils in the CANA+MI group mice was significantly reduced compared to the MI group,with associated proteins p-P65,p-IκBα.The expression level was significantly reduced.Conclusion Canagliflozin inhibits cardiac inflammatory response after MI and reduces cell apoptosis.