Protective Effects of Liriodendrin on Myocardial Infarction-Induced Fibrosis in Rats via the PI3K/Akt Autophagy Pathway: A Network Pharmacology Study
- 作者: Zhang P.1, Liu X.2, Yu X.2, Zhuo Y.3, Li D.3, Yang L.3, Lu Y.4
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隶属关系:
- Department of Cardiology, Tianjin Nankai Hospital
- Graduate School, Tianjin University of Traditional Chinese Medicine
- Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital
- Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital
- 期: 卷 27, 编号 11 (2024)
- 页面: 1566-1575
- 栏目: Chemistry
- URL: https://rjeid.com/1386-2073/article/view/643872
- DOI: https://doi.org/10.2174/1386207326666230717155641
- ID: 643872
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详细
Background:Liriodendrin (LIR) has been reported to improve cardiac function in rats following myocardial infarction. However, its role and mechanism in reparative myocardial fibrosis remain unclear.
Methods:In this study, a rat model of myocardial fibrosis was established via left anterior descending artery ligation and randomly divided into three groups (n = 6 per group): sham-operated, myocardial infarction, and LIR intervention (100 mg/kg/day) groups. The pharmacological effects of LIR were assessed using echocardiography, hematoxylin, and eosin (H&E) staining, and Masson staining. Network pharmacology and bioinformatics were utilized to identify potential mechanisms of LIR, which were further validated via western blot analysis.
Results:Our findings demonstrated that LIR improved cardiac function, histology scores, and col lagen volume fraction. Moreover, LIR downregulated the expression of Beclin-1, LC3-II/LC3-I while upregulating the expression of p62, indicating LIR-inhibited autophagy in the heart after myocardial infarction. Further analysis revealed that the PI3K/Akt signaling pathway was significantly enriched and validated by western blot. This analysis suggested that the ratios of p- PI3K/PI3K, p-Akt/Akt, and p-mTOR/mTOR were significantly increased.
Conclusion:LIR may attenuate myocardial infarction-induced fibrosis in rats by inhibiting excessive myocardial autophagy, with the potential mechanism involving the activation of the PI3K/Akt/mTOR pathway.
作者简介
Ping Zhang
Department of Cardiology, Tianjin Nankai Hospital
Email: info@benthamscience.net
Xuanming Liu
Graduate School, Tianjin University of Traditional Chinese Medicine
Email: info@benthamscience.net
Xin Yu
Graduate School, Tianjin University of Traditional Chinese Medicine
Email: info@benthamscience.net
Yuzhen Zhuo
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital
Email: info@benthamscience.net
Dihua Li
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital
Email: info@benthamscience.net
Lei Yang
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital
编辑信件的主要联系方式.
Email: info@benthamscience.net
Yanmin Lu
Tianjin Key Laboratory of Acute Abdomen Disease Associated Organ Injury and ITCWM Repair Abdomen Disease Associated Organ Injury and ITCWM Repair, Tianjin Nankai Hospital
编辑信件的主要联系方式.
Email: info@benthamscience.net
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