DL-炔丙基甘氨酸可通过抑制内质网应激来预防由慢性间歇性缺氧引起的心肌损伤。,Sleep and Breathing

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DL-炔丙基甘氨酸可通过抑制内质网应激来预防由慢性间歇性缺氧引起的心肌损伤。
Sleep and Breathing ( IF 2.1 ) Pub Date : 2018-05-18 , DOI: 10.1007/s11325-018-1656-0
Xiufang Zhou ₁ , Si Tang ₁ , Ke Hu ₁ , Zhan Zhang ₁ , Pei Liu ₁ , Yuchuan Luo ₁ , Jing Kang ₁ , Lifang Xu ₁

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背景技术慢性间歇性缺氧（CIH）是阻塞性睡眠呼吸暂停综合症（OSAS）引起器官损伤的重要发病机制，它与心肌损伤相关，例如左心功能不全，细胞凋亡和氧化应激。内源性硫化氢（H2S）在维持心血管功能中起重要作用。许多研究表明，外源性H2S对各种心血管疾病引起的心肌损伤具有保护作用，而抑制内源性H2S的产生则具有相反的作用。然而，DL-炔丙基甘氨酸（PAG）是一种有效的胱硫醚γ-裂合酶（CSE）合成的H2S抑制剂，对调节心肌损伤的作用仍存在争议。目的本研究旨在探讨PAG对CIH诱导的大鼠心肌损伤的影响。方法将Sprague-Dawley大鼠随机分为正常对照组（NC），CIH组，NC + PAG组和CIH + PAG组。建立大鼠CIH模型后，检测其血压，左心室功能，氧化应激，细胞凋亡和内质网（ER）应激水平。结果在NC大鼠中，PAG对血压无影响，但可引起心肌功能障碍，并上调氧化应激和心肌细胞凋亡。在CIH + PAG组中，与CIH组相比，PAG预处理可显着降低血压并改善左心室射血分数（LVEF）和左心室分数缩短（LVFS）。与CIH组相比，CIH + PAG组的氧化应激，细胞凋亡和ER应激水平显着降低。结论这些结果表明PAG可以通过抑制内质网应激来保护心肌免受CIH诱导的损伤。

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DL-Propargylglycine protects against myocardial injury induced by chronic intermittent hypoxia through inhibition of endoplasmic reticulum stress.

BACKGROUND Chronic intermittent hypoxia (CIH), an important basis of the pathogenesis of organ damage induced by obstructive sleep apnea syndrome (OSAS), is associated with myocardial injury, such as left ventricular dysfunction, apoptosis, and oxidative stress. Endogenous hydrogen sulfide (H2S) plays an important role in maintaining cardiovascular functions. Many studies have demonstrated that exogenous H2S has protective effects against myocardial injury induced by various cardiovascular diseases, and inhibiting the generation of endogenous H2S has opposite effects. However, the effect of DL-propargylglycine (PAG), an effective inhibitor of cystathionine γ-lyase (CSE)-synthesized H2S, on the regulation myocardial injury remains controversial. PURPOSE The present study was aimed to explore the influence of PAG on myocardial injury induced in rats by CIH. METHODS Sprague-Dawley rats were randomly divided into a normal control (NC) group, a CIH group, a NC + PAG group, and a CIH + PAG group. After establishing the CIH model in rats, blood pressure, left ventricular function, oxidative stress, apoptosis, and the level of endoplasmic reticulum (ER) stress were detected. RESULTS In NC rats, PAG had no effect on blood pressure, but induced myocardial dysfunction and up-regulated oxidative stress and apoptosis of the myocardium. In the CIH + PAG group, pretreatment with PAG significantly reduced blood pressure and improved the left ventricular ejection fraction (LVEF) and the left ventricular fractional shortening (LVFS) compared to the CIH group. Significantly lower levels of oxidative stress, apoptosis, and the ER stress were detected in the CIH + PAG group than in the CIH group. CONCLUSION These results suggest that PAG can protect the myocardium against CIH-induced injury through inhibition of endoplasmic reticulum stress.

更新日期：2019-11-01

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