Cardiac Shock Wave Therapy Improves Ventricular Function by Relieving Fibrosis Through PI3K/Akt Signaling Pathway: Evidence From a Rat Model of Post-infarction Heart Failure.
Cardiac Shock Wave Therapy Improves Ventricular Function by Relieving Fibrosis Through PI3K/Akt Signaling Pathway: Evidence From a Rat Model of Post-infarction Heart Failure.
复制标题
心脏冲击波疗法通过 PI3K/Akt 信号通路缓解纤维化来改善心室功能：来自梗塞后心力衰竭大鼠模型的证据
DOI：
10.3389/fcvm.2021.693875
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发表时间：
2021
影响因子：
3.6
通讯作者：
Yang P
中科院分区：
文献类型：
--
作者：
Wang L;Tian X;Cao Y;Ma X;Shang L;Li H;Zhang X;Deng F;Li S;Guo T;Yang P
目的：累积的研究已经确定了心脏冲击波治疗（CSWT）治疗急性心肌梗死（AMI）后心力衰竭的有效性，但关于CSWT抗纤维化的有益作用及其潜在机制的讨论很少。在本研究中，我们研究了CSWT是否可以减轻ami后纤维化，并进一步探讨了分子机制。方法：建立结扎左冠状动脉前降支致大鼠心力衰竭模型，并进行超声心动图验证。将符合条件的动物随机分为5组：假手术组、HF组、HF + CSWT组、HF + LY294002组和HF + CSWT + LY294002组。测定各组心脏重量、血清BNP、NT-pro BNP水平及超声心动图参数，评价各组心功能。马松三色染色法评估纤维化区域的比例。采用RT-PCR、免疫组化和免疫荧光法检测CD34、αSMA的表达水平，免疫组化和Western blotting检测PI3K/Akt的表达水平。结果：与HF组相比，CSWT的应用显著改善了心功能，降低了心肌纤维化，降低了CD34和αSMA的水平。与HF组相比，CSWT导致p-PI3K和p-Akt表达水平显著升高，PI3K/Akt通路的抑制消除了CSWT所观察到的有益作用。结论：CSWT可通过激活PI3K/Akt信号通路，促进AMI所致心肌纤维化的缓解。
Objection: Cumulative studies have identified the effectiveness of cardiac shock wave therapy (CSWT) in treating heart failure after acute myocardial infarction (AMI), but little have been discussed with regard to the beneficial effects of CSWT on anti-fibrosis along with the underlying mechanism. In this study, we investigated whether CSWT could reduce post-AMI fibrosis and further explored the molecular mechanism. Methods: Rat heart failure (HF) models induced by ligating the left anterior descending coronary artery were established and validated by echocardiography. Eligible animals were randomly categorized into five groups: the sham group, the HF group, the HF + CSWT group, the HF + LY294002 group, and the HF + CSWT + LY294002 group. The cardiac weight, serum level of BNP, NT-pro BNP and echocardiography parameters were measured to assess cardiac function in different groups. Masson's trichrome staining was used to assess the proportions of the fibrotic area. The expression level of CD34, αSMA was measured by RT-PCR, Immunohistochemistry and Immunofluorescent analyses and the level of PI3K/Akt was quantified by Immunohistochemistry and Western blotting. Results: The application of CSWT significantly improved cardiac function and reduced myocardial fibrosis and level of CD34 and αSMA, compared to the HF group. CSWT led to significant elevations of p-PI3K and p-Akt expression levels compared to that of the HF group and the inhibition of the PI3K/Akt pathway abolished the observed beneficial effects of CSWT. Conclusion: CSWT can facilitate the alleviation of cardiac fibrosis induced by AMI through the activation of PI3K/Akt signaling pathway.