首页|Tongxinluo Activates PI3K/AKT Signaling Pathway to inhibit Endothelial Mesenchymal Transition and Attenuate Myocardial Fibrosis after Ischemia-Reperfusion in Mice

Tongxinluo Activates PI3K/AKT Signaling Pathway to inhibit Endothelial Mesenchymal Transition and Attenuate Myocardial Fibrosis after Ischemia-Reperfusion in Mice

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Objective:To investigate the potential role of Tongxinluo(TXL)in attenuating myocardial fibrosis after myocardial ischemia-reperfusion injury(MIRI)in mice.Methods:A MIRI mouse model was established by left anterior descending coronary artery ligation for 45 min.According to a random number table,66 mice were randomly divided into 6 groups(n=11 per group):the sham group,the model group,the LY-294002 group,the TXL group,the TXL+LY-294002 group and the benazepril(BNPL)group.The day after modeling,TXL and BNPL were administered by gavage.Intraperitoneal injection of LY-294002 was performed twice a week for 4 consecutive weeks.Echocardiography was used to measure cardiac function in mice.Masson staining was used to evaluate the degree of myocardial fibrosis in mice.Qualitative and quantitative analysis of endothelial mesenchymal transition(EndMT)after MIRI was performed by immunohistochemistry,immunofluorescence staining and flow cytometry,respectively.The protein expressions of platelet endothelial cell adhesion molecule-1(CD31),α-smoth muscle actin(α-SMA),phosphatidylinositol-3-kinase(PI3K)and phospho protein kinase B(p-AKT)were assessed using Western blot.Results:TXL improved cardiac function in MIRI mice,reduced the degree of myocardial fibrosis,increased the expression of CD31 and inhibited the expression of α-SMA,thus inhibited the occurrence of EndMT(P＜0.05 or P＜0.01).TXL significantly increased the protein expressions of PI3K and p-AKT(P＜0.05 or P＜0.01).There was no significant difference between TXL and BNPL group(P＞0.05).In addition,the use of the PI3K/AKT pathway-specific inhibitor LY-294002 to block this pathway and combination with TXL intervention,eliminated the protective effect of TXL,further supporting the protective effect of TXL.Conclusion:TXL activated the PI3K/AKT signaling pathway to inhibit EndMT and attenuated myocardial fibrosis after MIRI in mice.

myocardial fibrosisendothelial mesenchymal transitionmyocardial ischemia-reperfusion injuryphosphatidylinositol-3-kinase/protein kinase B(PI3K/AKT)pathway

WEI Ya-ru、HOU Yun-long、YIN Yu-jie、LI Zhen、LIU Yi、HAN Ning-xin、WANG Zi-xuan、LIU Lu、WANG Xiao-qi、HAO Yuan-jie、MA Kun、GU Jiao-jiao、JIA Zhen-hua

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Graduate School,Hebei University of Chinese Medicine,Shijiazhuang(050090),China

Shijiazhuang Yiling Pharmaceutical New Drug Evaluation Center,Shijiazhuang(050035),China

Hebei Institute of Integrated Traditional and Western Medicine,Shijiazhuang(050035),China

National Key Laboratory for Innovation and Transformation of Luobing Theory,Shijiazhuang(050035),China

Department of Cardiology,Hebei Yiling Hospital,Shijiazhuang(050091),China

Graduate School,Hebei Medical University,Shijiazhuang(050017),China

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National Natural Science Foundation of ChinaTraditional Chinese Medicine Innovation Project of Hebei ProvinceHigh-Level Talent Funding Program of Hebei

81973692223777120DE2020100001

2024

10.1007/s11655-024-3652-5

中国结合医学杂志(英文版)
中国中西医结合学会 中国中医研究院

中国结合医学杂志(英文版)

CSTPCD
影响因子：1.056
ISSN：1672-0415
年,卷(期)：2024.30(7)