BACKGROUND: To investigate the impact of autophagy on cardiomyocyte membrane connexin 43 (Cx43) expression, distribution, and phosphorylation in myocardial ischemia-reperfusion injury (MI/RI). METHODS: Twenty-four male SD rats were randomly divided into a sham operation group, a chloroquine (CQ) + sham operation group, an I/R group, and a CQ + I/R group. The MI/RI model was established by reversible ligation of the left anterior descending coronary artery to induce ischemia for 30 min and reperfusion for 2 h. The left ventricular infarct size was measured by TTC (2,3,5-triphenyltetrazolium chloride) and Evans blue double staining. Cardiac troponin I (cTnI) content was detected by automatic biochemical analyzer. Autophagy related gene Beclin1, Cx43, and p-Cx43 protein expressions were tested by western blot. Cx43 and p-Cx43 distributions in ventricular myocardium were observed by immunofluorescence analysis. RESULTS: Compared with the I/R group, the left ventricular infarct size, serum cTnI content, reperfusion arrhythmia severity, and in vivo induced ventricular fibrillation threshold, and Beclin-1 protein expression were significantly reduced in CQ + I/R group (P < 0.05). Compared with the SH group, Beclin-1 protein expression was significantly enhanced, while Cx43 and p-Cx43 levels were obviously downregulated in the I/R group. Beclin-1 protein declined, whereas Cx43 and p-Cx43 levels enhanced in CQ + I/R group compared with the I/R group. CONCLUSION: Autophagy may reduce myocardial ischemia-reperfusion injury and malignant arrhythmia by improving the acute remodeling of myocardial cell membrane Cx43. IJCEP
BACKGROUND: To investigate the impact of autophagy on cardiomyocyte membrane connexin 43 (Cx43) expression, distribution, and phosphorylation in myocardial ischemia-reperfusion injury (MI/RI). METHODS: Twenty-four male SD rats were randomly divided into a sham operation group, a chloroquine (CQ) + sham operation group, an I/R group, and a CQ + I/R group. The MI/RI model was established by reversible ligation of the left anterior descending coronary artery to induce ischemia for 30 min and reperfusion for 2 h. The left ventricular infarct size was measured by TTC (2,3,5-triphenyltetrazolium chloride) and Evans blue double staining. Cardiac troponin I (cTnI) content was detected by automatic biochemical analyzer. Autophagy related gene Beclin1, Cx43, and p-Cx43 protein expressions were tested by western blot. Cx43 and p-Cx43 distributions in ventricular myocardium were observed by immunofluorescence analysis. RESULTS: Compared with the I/R group, the left ventricular infarct size, serum cTnI content, reperfusion arrhythmia severity, and in vivo induced ventricular fibrillation threshold, and Beclin-1 protein expression were significantly reduced in CQ + I/R group (P < 0.05). Compared with the SH group, Beclin-1 protein expression was significantly enhanced, while Cx43 and p-Cx43 levels were obviously downregulated in the I/R group. Beclin-1 protein declined, whereas Cx43 and p-Cx43 levels enhanced in CQ + I/R group compared with the I/R group. CONCLUSION: Autophagy may reduce myocardial ischemia-reperfusion injury and malignant arrhythmia by improving the acute remodeling of myocardial cell membrane Cx43. IJCEP