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Archive > Volume 17 Issue 3 > 2025,17(3):548-554. DOI:https://doi.org/10.1016/j.chmed.2024.03.003 Prev Next

復(fù)方丹參片通過(guò)AMPK/mTOR信號(hào)通路調(diào)控自噬改善心肌缺血/再灌注損傷誘導(dǎo)的心室重構(gòu)

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Compound Danshen Tablets ameliorate myocardial ischemia/reperfusion injury-induced ventricular remodeling by regulating autophagy via AMPK/mTOR signaling pathway

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    摘要:
    目的：心肌缺血/再灌注損傷（MI/RI）導(dǎo)致的左心室重構(gòu)是一種常見(jiàn)的心功能不全。越來(lái)越多的證據(jù)表明，自噬在防止心室重構(gòu)中起著至關(guān)重要的作用。本研究旨在探討復(fù)方丹參片（CDT）對(duì)心室重構(gòu)的改善作用及自噬是否為其潛在機(jī)制。 方法：將大鼠左前降支暫時(shí)結(jié)扎30min，建立MI/RI模型。再灌注28 d誘導(dǎo)心室重構(gòu)，在此期間給予MI/RI大鼠CDT（300 mg/kg和600 mg/kg）、阿托伐他?。? mg/kg）和地爾硫?（16 mg/kg）。超聲心動(dòng)檢測(cè)大鼠心臟結(jié)構(gòu)和功能。免疫組織化學(xué)、Masson三色染色和蘇木精-伊紅（H & E）染色用于評(píng)價(jià)心臟組織的纖維化和組織學(xué)改變。Western blot檢測(cè)自噬相關(guān)蛋白的表達(dá)。 結(jié)果：CDT減輕了MI/RI引起的心功能不全、結(jié)構(gòu)改變、組織病理學(xué)改變和纖維化。CDT可顯著提高M(jìn)I/RI大鼠心臟Beclin1和微管相關(guān)蛋白1輕鏈3β（LC3β）的水平，降低p62的水平。此外，CDT顯著增加腺苷酸活化蛋白激（AMPK）的磷酸化，并抑制哺乳動(dòng)物雷帕霉素靶分子（mTOR）磷酸化。 結(jié)論：CDT通過(guò)AMPK/mTOR信號(hào)通路激活自噬，改善自噬流，從而改善MI/RI誘導(dǎo)的心室重構(gòu)。

    Abstract:
    Objective: Left ventricular remodeling induced by myocardial ischemia/reperfusion injury (MI/RI) is a common cardiac dysfunction. Accumulating evidence has demonstrated that autophagy plays a vital role in protecting against ventricular remodeling. This study aims to investigate the performance of Compound Danshen Tablets (CDT) in rescuing ventricular remodeling and whether autophagy as the potential mechanism. Methods: The left anterior descending arteries of rats were temporarily ligated for 30 min to construct the MI/RI model. Ventricular remodeling was induced by reperfusion for 28 d, during which the MI/RI rats were administered CDT (300 mg/kg and 600 mg/kg), atorvastatin (2 mg/kg), and diltiazem (16 mg/kg). Cardiac function and structure were examined by echocardiography. Immunohistochemistry, Masson’s trichrome staining, and hematoxylin-eosin (HE) staining were utilized to assess the fibrosis and histological alterations in the heart tissue. The expression of autophagy-related proteins was detected using Western blotting. Results: CDT attenuated the cardiac dysfunction, structural changes, histopathological changes and fibrosis induced by MI/RI. CDT significantly enhanced the level of Beclin1 and microtubule-associated protein 1 light chain 3 beta (LC3b), and reduced p62 levels in MI/RI rats. Moreover, CDT significantly increased the phosphorylation of adenosine monophosphate-activated protein kinase (AMPK) and inhibited mammalian target of rapamycin (mTOR) phosphorylation. Conclusion: CDT ameliorated MI/RI-induced ventricular remodeling by activating autophagy and improving autophagic flux via the AMPK/mTOR signaling pathway.

    關(guān)鍵詞:
    AMPK/mTOR信號(hào)通路;自噬;復(fù)方丹參片;心肌缺血/再灌注損傷;心室重構(gòu)

    Keywords:


    Project Supported:
    This work was supported by Guangdong Province Key Field R&D Program Project (No. 2020B111111002) and the National Natural Science Foundation of China (No. U1812403-5-3; 81891012).

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