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首页> 外文期刊>RSC Advances >Morroniside alleviates coxsackievirus B3-induced myocardial damage apoptosis via restraining NLRP3 inflammasome activation
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Morroniside alleviates coxsackievirus B3-induced myocardial damage apoptosis via restraining NLRP3 inflammasome activation

机译：莫罗尼酰胺通过抑制NLRP3炎性激活来缓解Coxsackievirus B3诱导的心肌损伤细胞凋亡

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摘要

Coxsackievirus B3 (CVB3)-induced myocardial damage always leads to serious heart failure by inducing cardiac injury. NLRP3 inflammasome activation has been identified as a central player in the pathogenesis of CVB3-induced viral myocarditis. Therefore, restraining NLRP3 inflammasome activation has been supposed to significantly alleviate the severity of myocardial damage and improve cardiac function. Morroniside (MR), one of the main iridoid glycosides, has the ability to depress the production of reactive oxygen species (ROS) and restrain the expression of caspase-3 and -9. Of importance, ROS and caspase are essential for NLRP3 inflammasome activation in response to CVB3 infection. Therefore, in the present study, MR was selected as a model drug to alleviate CVB3-induced myocardial damage. The results of cardiac function index determination showed that abnormal indexes including mean arterial pressure, heart rate, and left ventricular systolic pressure of myocardial damage rats could be recovered by treating with MR. Such results can be further verified by histopathological evaluation, with the heart tissues of CVB3-infected rats displaying the most amount of H&E and TUNEL positive cells. The underlying mechanism by which MR improves the cardiac function was subsequently investigated. The detection of various gene levels indicated that NLRP3 inflammasome activation was inhibited by MR through down-regulating the expression of pro-inflammatory cytokines: interleukin (IL)-beta and IL-18, the pivotal factors that lead to inflammatory responses. More importantly, the related genes, cardiac function indexes, and various myocardial damage markers of normal rats treated with MR did not exhibit any obvious changes compared with the control group, indicating a satisfactory biocompatibility of MR. In summary, MR holds a great potential in the alleviation of CVB3-induced myocardial damage with a negligible cytotoxicity to normal heart tissues.
机译：CoxSackeivirus B3（CVB3） - 诱导心肌损伤总是通过诱导心脏损伤导致严重的心力衰竭。 NLRP3炎症组活化已被鉴定为CVB3诱导的病毒心肌炎的发病机制中的中央球员。因此，抑制NLRP3炎症组活化已经应该显着减轻心肌损伤的严重程度并改善心脏功能。 Morroniside（MR）是主要的虹膜糖苷之一，具有抑制反应性氧物质（ROS）的产生并抑制Caspase-3和-9的表达。重要的是，ROS和Caspase响应CVB3感染的NLRP3炎症组活化是必不可少的。因此，在本研究中，先生被选为模型药物以缓解CVB3诱导的心肌损伤。心功能指数测定结果表明，通过MR治疗，可以通过治疗方法来回收包括平均动脉压，心率和左心室收缩压的异常指标。通过组织病理学评估可以进一步验证这些结果，其中CVB3感染大鼠的心脏组织显示最多的H＆E和TUNEL阳性细胞。随后调查了先生提高心功能的潜在机制。各种基因水平的检测表明，MR通过下调促炎细胞因子的表达：白细胞介素（IL）-Beta和IL-18，致炎症反应的关键因素抑制了NLRP3炎症组活化。更重要的是，与对照组相比，用MR治疗的正常大鼠的相关基因，心脏功能指标和各种心肌损伤标记表明MR的令人满意的生物相容性，没有表现出任何明显的变化。总之，MR对CVB3诱导的心肌损伤具有巨大的潜力，以常规心脏组织具有可忽略的细胞毒性。

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  • 来源
    《RSC Advances》 |2019年第3期|共8页
  • 作者

    Li Weidong; Chen Mao; Xu Lishuai; Lv Zhan; Chen Li; Li Yiling; He WenFen;

  • 作者单位

    Sichuan Univ West China Hosp Dept Cardiol 37 Guoxue Alley Chengdu 610041 Sichuan Peoples R China;

    Sichuan Univ West China Hosp Dept Cardiol 37 Guoxue Alley Chengdu 610041 Sichuan Peoples R China;

    North Sichuan Med Coll Dept Ophthalmol Affiliated Hosp Nanchong Sichuan Peoples R China;

    North Sichuan Med Coll Dept Cardiol Affiliated Hosp Nanchong Sichuan Peoples R China;

    North Sichuan Med Coll Dept Cardiol Affiliated Hosp Nanchong Sichuan Peoples R China;

    North Sichuan Med Coll Dept Cardiol Affiliated Hosp 2 Nanchong Sichuan Peoples R China;

    North Sichuan Med Coll Dept Cardiol Affiliated Hosp Nanchong Sichuan Peoples R China;

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  • 中图分类 化学;
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