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QiShenYiQi pill activates autophagy to attenuate reactive myocardial fibrosis via the PI3K/AKT/mTOR pathway
被引:4
|作者:
Lv, Shichao
[1
,2
]
Yuan, Peng
[1
]
Lu, Chunmiao
[3
]
Dong, Jianping
[4
]
Li, Meng
[1
]
Qu, Fan
[1
]
Zhu, Yaping
[1
]
Zhang, Junping
[1
]
机构:
[1] Tianjin Univ Tradit Chinese Med, Teaching Hosp 1, Tianjin 300193, Peoples R China
[2] Tianjin Key Lab Tradit Res TCM Prescript & Syndro, Tianjin 300193, Peoples R China
[3] Jiashan Hosp Tradit Chinese Med, Jiaxing 314100, Zhejiang, Peoples R China
[4] Hlth Ctr Balitai Town, Tianjin 300350, Peoples R China
来源:
基金:
中国国家自然科学基金;
关键词:
reactive myocardial fibrosis;
traditional Chinese medicine;
autophagy;
PI3K/AKT/mTOR pathway;
LEFT-VENTRICULAR HYPERTROPHY;
DISEASE;
INJURY;
HYPERTENSION;
GROWTH;
CELLS;
RATS;
D O I:
暂无
中图分类号:
Q2 [细胞生物学];
学科分类号:
071009 ;
090102 ;
摘要:
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.
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页码:5525 / 5538
页数:14
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