Effects of Linggui Zhugan Decoction on Left Ventricular Myocardial Fibrosis and PI3K/AKT Signaling Pathway in Rats with Chronic Heart Failure
10.13359/j.cnki.gzxbtcm.2025.09.027
- VernacularTitle:苓桂术甘汤对慢性心力衰竭大鼠左心室心肌纤维化及PI3K/AKT信号通路的影响
- Author:
Jiyuan LU
1
;
Mengke JIANG
Author Information
1. 常州市中医医院心血管一科,江苏常州 213000
- Keywords:
Linggui Zhugan Decoction;
chronic heart failure(CHF);
PI3K/AKT signaling pathway;
myocardial fibrosis;
rats
- From:
Journal of Guangzhou University of Traditional Chinese Medicine
2025;42(9):2280-2287
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the effects of Linggui Zhugan Decoction(LGZGD)on left ventricular myocardial fibrosis and the phosphatidylinositol 3-kinase(PI3K)/protein kinase B(AKT)signaling pathway in rats with chronic heart failure(CHF).Methods A rat model of CHF with myocardial fibrosis was established via coronary artery ligation.Rats were randomly divided into sham-operated,model,LGZGD low/medium/high-dose,and Captopril groups,with 10 rats in each group.After treatment,cardiac function was assessed by echocardiography.Myocardial histopathology was examined using hematoxylin-eosin(HE)staining(with cardiomyocyte cross-sectional area calculated),while collagen deposition was evaluated via Masson's trichrome staining(collagen volume fraction quantified).ELISA was used to measure myocardial TNF-α and IL-6 levels.Western Blot was used to analyze expression of fibrosis markers(TGF-β1,α-SMA,collagen Ⅰ/Ⅲ)and PI3K/AKT pathway components(p-PI3K,p-AKT,p-mTOR).Results Compared with the sham-operated group,the model group showed significantly reduced LVEF and LVFS levels,as well as significantly increased myocardial cell cross-sectional area,collagen deposition area ratio,myocardial tissue TNF-α and IL-6 levels,and TGF-β1,α-SMA,collagen Ⅰ,collagen Ⅲ,p-PI3K,p-AKT,and p-mTOR levels,with statistically significant differences(P＜0.01);compared with the model group,the Captopril group and the medium-and high-dose groups of LGZGD showed significantly increased LVEF and LVFS,as well as significantly increased myocardial cell cross-sectional area,collagen deposition area ratio,TNF-α and IL-6 levels,and TGF-β1,α-SMA,collagen Ⅰ,collagen Ⅲ,p-PI3K,p-AKT,and p-mTOR levels were significantly reduced,with statistically significant differences(P＜0.01);compared with the Captopril group,the high-dose group of LGZGD showed a significant increase in LVEF and LVFS,as well as a significant decrease in myocardial cell cross-sectional area,collagen deposition area ratio,TNF-α,IL-61evels,andTGF-β1,α-SMA,collagen Ⅰ,collagen Ⅲ,p-PI3K,p-AKT,and p-mTOR levels were significantly reduced,with statistically significant differences(P＜0.01).Conclusion LGZGD ameliorates left ventricular myocardial fibrosis and pathological damage in CHF rats,potentially through inhibition of the PI3K/AKT signaling pathway.
