Effect of WenXin KeLi on Improvement of Arrhythmia after Myocardial Infarction by Intervening PI3K-AKT-mTOR Autophagy Pathway

Figure 6

The increased risk of arrhythmia after MI was related to the overactivation of autophagy after MI. WenXin KeLi could activate the PI3K-AKT-mTOR signal pathway, up-regulate the phosphorylation expression of PI3K, AKT, and mTOR proteins, inhibit the level of cardiac autophagy, reduce the expression of Beclin1 and LC3-II proteins, increase the expression of the P62 protein, and reduce the risk of arrhythmia after MI. The increased risk of arrhythmia after MI was related to the decreased expression of CX43 after MI. The internalization and degradation of CX43 increased after MI. WenXin KeLi could significantly increase the expression of CX43, reduce gap junction degradation and reduce the risk of arrhythmia after MI.