Electroacupuncture as a promising therapeutic strategy for doxorubicin-induced heart failure: Insights into the PI3K/AKT/mTOR/ULK1 and AMPK /mTOR /ULK1 pathways

IF 5.4 2区医学 Q1 BIOPHYSICS Colloids and Surfaces B: Biointerfaces Pub Date : 2025-02-26 DOI:10.1016/j.colsurfb.2025.114590

Peng Chao , Xueqin Zhang , Lei Zhang, Zhengyang Han, Runda Jie, Pingxiu Duan, Min Cao, Aiping Yang

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Abstract

Background

Electroacupuncture (EA), a traditional Chinese medicine therapy, exhibits cardioprotective and therapeutic effects against cardiac injury. However, the precise mechanisms underlying these benefits remain unclear.

Purpose

The aim of this study is to examine the impact of EA on Doxorubicin-Induced heart failure and elucidate the mechanisms involved.

Methods

C57BL/6 mice were randomly assigned to six experimental groups, including a control group, a DCM group, a DCM group receiving non-acupoint EA (NEA), and a DCM group receiving acupoint EA (EA). The cardiac function, levels of inflammatory factors, and markers of apoptosis were assessed both in vivo and in vitro. The presence of AMPK/mTOR/ULK1(Ser317) and PI3K/AKT/mTOR/ULK1(Ser757) was confirmed.

Results

EA stimulation significantly improved cardiac function, as evidenced by increased left ventricular ejection fraction (LVEF), E/A ratio, and fractional shortening (FS%) compared to the DCM group (p < 0.05). After EA stimulation, the phosphorylation levels of PI3K/AKT increase, leading to elevated expression of mTOR/ULK1(Ser757), which ultimately inhibited the expression of apoptosis-related proteins and inflammatory factors. Simultaneously, EA stimulation could inhibit the phosphorylation levels of AMPK, reducing the expression of mTOR/ULK1(Ser317), and thereby also inhibiting the expression of apoptosis-related proteins and inflammatory factors.

Conclusions

This study showed that EA stimulation can counteract myocardial damage caused by apoptosis and inflammation, thereby significantly improving cardiac function and prognosis in HF mice. The mechanism may be that EA stimulation activates the PI3K/AKT/mTOR/ULK1(ser757) pathway and inhibits the AMPK/ULK1(ser317) pathway. EA stimulation exerts the same effect by regulating these two pathways in different directions, ultimately reducing myocardial cell apoptosis and cardiac inflammation.

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来源期刊

Colloids and Surfaces B: Biointerfaces 生物-材料科学：生物材料

CiteScore

11.10

自引率

3.40%

发文量

730

审稿时长

42 days

期刊介绍： Colloids and Surfaces B: Biointerfaces is an international journal devoted to fundamental and applied research on colloid and interfacial phenomena in relation to systems of biological origin, having particular relevance to the medical, pharmaceutical, biotechnological, food and cosmetic fields. Submissions that: (1) deal solely with biological phenomena and do not describe the physico-chemical or colloid-chemical background and/or mechanism of the phenomena, and (2) deal solely with colloid/interfacial phenomena and do not have appropriate biological content or relevance, are outside the scope of the journal and will not be considered for publication. The journal publishes regular research papers, reviews, short communications and invited perspective articles, called BioInterface Perspectives. The BioInterface Perspective provide researchers the opportunity to review their own work, as well as provide insight into the work of others that inspired and influenced the author. Regular articles should have a maximum total length of 6,000 words. In addition, a (combined) maximum of 8 normal-sized figures and/or tables is allowed (so for instance 3 tables and 5 figures). For multiple-panel figures each set of two panels equates to one figure. Short communications should not exceed half of the above. It is required to give on the article cover page a short statistical summary of the article listing the total number of words and tables/figures.