First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin, China.
Tianjin Key Laboratory of Traditional Research of TCM Prescription and Syndrome, Tianjin, China.
J Cell Mol Med. 2020 Oct;24(19):11283-11293. doi: 10.1111/jcmm.15695. Epub 2020 Sep 2.
QiShenYiQi pill (QSYQ), a traditional Chinese medicine, is well known for improving the myocardial remodelling, but the dose-effect relationship of its intervention in the reparative myocardial fibrosis is still unclear. We investigated the effect of QSYQ on the reparative myocardial fibrosis in cardiac myosin-induced rats and explored its mechanism of action by regulating autophagy. The results indicated that QSYQ increased LVEF and LVFS, and decreased the LVEDD, LVESD, HMI, LVMI, myocardial inflammation histology score, and collagen volume fraction in a dose-dependent manner. In addition, QSYQ declined the number of autophagosomes, down-regulated the expression of myocardial Beclin-1 and LC3B, up-regulated the expression of myocardial p62 and increased the ratios of myocardial p-PI3K/PI3K, p-Akt/Akt and p-mTOR/mTOR. We provided evidence for that QSYQ could inhibit excessive myocardial autophagy by regulating the PI3K/Akt-mTOR pathway and can be a potential therapeutic approach in treating the cardiovascular diseases such as myocarditis and dilated cardiomyopathy.
芪参益气滴丸（QSYQ）是一种中药，以改善心肌重构而闻名，但它对修复性心肌纤维化的干预的剂量-效应关系尚不清楚。我们研究了 QSYQ 对心肌肌球蛋白诱导的大鼠修复性心肌纤维化的影响，并通过调节自噬来探讨其作用机制。结果表明，QSYQ 可增加 LVEF 和 LVFS，并降低 LVEDD、LVESD、HMI、LVMI、心肌炎症组织学评分和胶原容积分数，呈剂量依赖性。此外，QSYQ 减少了自噬体的数量，下调了心肌 Beclin-1 和 LC3B 的表达，上调了心肌 p62 的表达，并增加了心肌 p-PI3K/PI3K、p-Akt/Akt 和 p-mTOR/mTOR 的比值。我们提供了证据表明，QSYQ 通过调节 PI3K/Akt-mTOR 通路可以抑制过度的心肌自噬，是治疗心肌炎和扩张型心肌病等心血管疾病的潜在治疗方法。
