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Research Paper|Volume 13, Issue 4|pp 5525—5538

QiShenYiQi pill activates autophagy to attenuate reactive myocardial fibrosis via the PI3K/AKT/mTOR pathway

Shichao Lv1,2, Peng Yuan1, Chunmiao Lu3, Jianping Dong4, Meng Li1, Fan Qu1, Yaping Zhu1, Junping Zhang1
  • 1First Teaching Hospital of Tianjin University of Traditional Chinese Medicine, Tianjin 300193, China
  • 2Tianjin Key Laboratory of Traditional Research of TCM Prescription and Syndrome, Tianjin 300193, China
  • 3Jiashan Hospital of Traditional Chinese Medicine, Jiaxing 314100, Zhejiang, China
  • 4Health Center of Balitai Town, Jinnan, Tianjin 300350, China
Received: August 27, 2020Accepted: November 20, 2020Published: February 11, 2021
https://doi.org/10.18632/aging.202482

Copyright: © 2021 Lv et al. This is an open access article distributed under the terms of the Creative Commons Attribution License (CC BY 3.0), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited.

Abstract

QiShenYiQi pill (QSYQ), a traditional Chinese medicine, is used to treat cardiovascular diseases. However, the dose-effect relationship of its intervention in the reactive myocardial fibrosis is elusive. In this work, rat models of reactive myocardial fibrosis induced by partial abdominal aortic coarctation were constructed and randomly classified into the model group, 3-methyladenine group, rapamycin group, QSYQ low-dose group, QSYQ medium-dose group, QSYQ high-dose group, and sham-operated rats (control group). We revealed that QSYQ lowered the heart mass index (HMI), left ventricular mass index (LVMI), and myocardial collagen volume fraction (CVF) levels in a dose-dependent mechanism. Additionally, QSYQ increased the number of autophagosomes, and the expression of myocardial Beclin-1 and LC3B. In contrast, it reduced the expression of myocardial p62 and decreased the ratios of myocardial p-PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR. In conclusion, our results have revealed that QSYQ impacts anti-reactive myocardial fibrosis in a dose-dependent mechanism which is mediated by the activation of myocardial autophagy via the PI3K/AKT/mTOR pathway.