不同强度的低强度脉冲超声通过调节心脏氧化应激和炎症反应不同程度地影响心肌缺血/再灌注损伤,Frontiers in Immunology

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不同强度的低强度脉冲超声通过调节心脏氧化应激和炎症反应不同程度地影响心肌缺血/再灌注损伤
Frontiers in Immunology ( IF 5.7 ) Pub Date : 2023-09-07 , DOI: 10.3389/fimmu.2023.1248056
Quan Cao _{1,

2} , Lian Liu ₃ , Yugang Hu ₂ , Sheng Cao ₂ , Tuantuan Tan ₂ , Xin Huang ₂ , Qing Deng ₂ , Jinling Chen ₂ , Ruiqiang Guo ₂ , Qing Zhou ₂

Affiliation

简介缺血性心脏病的患病率已达到全球大流行水平。早期血运重建是目前治疗缺血性心脏病最有效的方法，但矛盾的是会引起心肌缺血/再灌注（MI/R）损伤。心脏炎症反应和氧化应激主要参与MI/R损伤的病理过程。低强度脉冲超声 (LIPUS) 已被证明可以通过防止许多疾病（包括心血管疾病）中的炎症反应和氧化应激来减少细胞损伤，但很少用于 MI/R 损伤。方法本研究旨在阐明 LIPUS 是否可以减轻 MI/R 损伤。 R通过减轻炎症反应和氧化应激损伤。同时，我们还试图确认哪种强度的 LIPUS 可能更适合改善 MI/R 损伤，并阐明信号传导机制。分别在 Sprague Dawley 大鼠和人多能干细胞来源的心肌细胞 (hPSC-CM) 中诱导 MI/R 和模拟缺血/再灌注 (SI/R)。根据方案进行LIPUS处理、生化测量、细胞死亡测定、心脏氧化应激和炎症反应的估计以及通过蛋白质印迹进行蛋白质检测。结果在我们的研究中，体内和体外，LIPUS为0.1 W/cm2（利普斯0.1）和0.5瓦/厘米2（利普斯0.5）在常氧条件下对心肌细胞没有显着差异。缺氧条件下，LIPUS可部分改善MI/R损伤、炎症反应和氧化应激0.5但 2.5 W/cm 的 LIPUS 会显着加剧2（利普斯2.5）体内和体外。MI/R 损伤心肌细胞中凋亡信号调节激酶 1 (ASK1)/c-Jun N 末端激酶 (JNK) 通路的激活得到部分纠正 LIPUS0.5结论我们的研究首先证明了不同强度的LIPUS通过调节心脏炎症反应和氧化应激来不同程度地影响MI/R损伤。对 ASK1/JNK 通路的调节是 LIPUS 的信号传导机制0.5发挥心脏保护作用。利普斯0.5在预防 MI/R 损伤方面有望实现临床转化。这对于患有 MI/R 损伤的患者来说将是巨大的福利。

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Low-intensity pulsed ultrasound of different intensities differently affects myocardial ischemia/reperfusion injury by modulating cardiac oxidative stress and inflammatory reaction

IntroductionThe prevalence of ischemic heart disease has reached pandemic levels worldwide. Early revascularization is currently the most effective therapy for ischemic heart diseases but paradoxically induces myocardial ischemia/reperfusion (MI/R) injury. Cardiac inflammatory reaction and oxidative stress are primarily involved in the pathology of MI/R injury. Low-intensity pulsed ultrasound (LIPUS) has been demonstrated to reduce cell injury by protecting against inflammatory reaction and oxidative stress in many diseases, including cardiovascular diseases, but rarely on MI/R injury.MethodsThis study was designed to clarify whether LIPUS alleviates MI/R injury by alleviating inflammatory reaction and oxidative stress. Simultaneously, we have also tried to confirm which intensity of the LIPUS might be more suitable to ameliorate the MI/R injury, as well as to clarify the signaling mechanisms. MI/R and simulated ischemia/reperfusion (SI/R) were respectively induced in Sprague Dawley rats and human pluripotent stem cell-derived cardiomyocytes (hPSC-CMs). LIPUS treatment, biochemical measurements, cell death assay, estimation of cardiac oxidative stress and inflammatory reaction, and protein detections by western blotting were performed according to the protocol.ResultsIn our study, both in vivo and in vitro, LIPUS of 0.1 W/cm2 (LIPUS0.1) and 0.5 W/cm2 (LIPUS0.5) make no significant difference in the cardiomyocytes under normoxic condition. Under the hypoxic condition, MI/R injury, inflammatory reaction, and oxidative stress were partially ameliorated by LIPUS0.5 but were significantly aggravated by LIPUS of 2.5 W/cm2 (LIPUS2.5) both in vivo and in vitro. The activation of the apoptosis signal-regulating kinase 1 (ASK1)/c-Jun N-terminal kinase (JNK) pathway in cardiomyocytes with MI/R injury was partly rectified LIPUS0.5 both in vivo and in vitro.ConclusionOur study firstly demonstrated that LIPUS of different intensities differently affects MI/R injury by regulating cardiac inflammatory reaction and oxidative stress. Modulations on the ASK1/JNK pathway are the signaling mechanism by which LIPUS0.5 exerts cardioprotective effects. LIPUS0.5 is promising for clinical translation in protecting against MI/R injury. This will be great welfare for patients suffering from MI/R injury.

更新日期：2023-09-07

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