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首页> 外文期刊>Cellular Physiology and Biochemistry >Protective Effects of Microrna-22 Against Endothelial Cell Injury by Targeting NLRP3 Through Suppression of the Inflammasome Signaling Pathway in a Rat Model of Coronary Heart Disease
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Protective Effects of Microrna-22 Against Endothelial Cell Injury by Targeting NLRP3 Through Suppression of the Inflammasome Signaling Pathway in a Rat Model of Coronary Heart Disease

机译：Microrna-22通过抑制炎性体信号通路在大鼠冠心病模型中靶向NLRP3对内皮细胞损伤的保护作用

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>Background/Aims: This study aimed to identify the role of microRNA-22 (miR-22) in endothelial cell (EC) injury in coronary heart disease (CHD) by targeting NLRP3 through the inflammasome signaling pathway. Methods: A total of 24 healthy male Sprague-Dawley (SD) rats were divided into normal and atherosclerosis groups. The atherosclerosis rats were assigned into blank, negative control (NC), miR-22 mimic, miR-22 inhibitor and miR-22 inhibitor + siNLRP3 groups. A luciferase reporter gene assay was used to detect the relationship between miR-22 and NLRP3. MiR-22 expression as well as NLRP3 and caspase-1 mRNA and protein expression were measured using quantitative real-time polymerase chain reaction (qRT-PCR) and Western blotting. The activity and apoptosis of coronary arterial endothelial cells (CAECs) were determined by MTT and Hoechst 33258. CAEC lumen formation was detected by a lumen formation assay. An enzyme-linked immunosorbent assay (ELISA) was used to detect IL-1?2, IL-6, IL-10 and IL-18 levels. Results: The results indicated that the atherosclerosis group significantly decreased miR-22 expression but increased NLRP3 and caspase-1 mRNA and protein expression. The cell survival rate was significantly increased in the miR-22 mimic group and significantly reduced in the miR-22 inhibitor group. The miR-22 mimic group displayed a lower apoptosis rate and more cells with obvious lumen walls and numerous tubular structures, while cells in the miR-22 inhibitor group were unable to form lumen walls and had a scattered distribution compared to the blank group. The ELISA showed that IL-1?2, IL-6 and IL-18 levels were markedly decreased, while IL-10 was clearly increased in the miR-22 mimic group. In contrast, in the miR-22 inhibitor group, IL-1?2, IL-6 and IL-18 levels were significantly increased, and IL-10 levels were decreased. Conclusion: Our findings indicated that miR-22 could lower the levels of pro-inflammatory cytokines by inhibiting the NLRP3 inflammasome pathway, which suppresses CAEC apoptosis and protects CAECs in rats with CHD.
机译：> 背景/目标： 这项研究旨在确定microRNA-22（miR-22）在冠心病（CHD）内皮细胞（EC）损伤中的作用）通过炎症小体信号通路靶向 NLRP3 。 方法： 总共将24只健康的雄性Sprague-Dawley（SD）大鼠分为正常组和动脉粥样硬化组。将动脉粥样硬化大鼠分为空白组，阴性对照（NC），miR-22模拟物，miR-22抑制剂和miR-22抑制剂+ siNLRP3组。荧光素酶报告基因测定用于检测miR-22和NLRP3之间的关系。使用定量实时聚合酶链反应（qRT-PCR）和Western印迹法测量MiR-22表达以及NLRP3和caspase-1 mRNA和蛋白质表达。通过MTT和Hoechst 33258测定冠状动脉内皮细胞（CAEC）的活性和凋亡。通过腔形成测定法检测CAEC腔形成。酶联免疫吸附试验（ELISA）用于检测IL-1？2，IL-6，IL-10和IL-18水平。 结果： 结果表明，动脉粥样硬化组显着降低miR-22表达，但增加NLRP3和caspase-1 mRNA和蛋白表达。在miR-22模拟组中，细胞存活率显着增加，而在miR-22抑制剂组中，细胞存活率显着降低。与空白组相比，miR-22模拟组显示出较低的凋亡率，并且具有明显的管腔壁和大量管状结构的细胞更多，而miR-22抑制剂组的细胞无法形成管腔壁并且具有分散的分布。 ELISA显示，miR-22模拟组的IL-1？2，IL-6和IL-18水平明显降低，而IL-10明显升高。相反，在miR-22抑制剂组中，IL-1β2，IL-6和IL-18水平显着升高，而IL-10水平降低。 结论： 我们的发现表明，miR-22可以通过抑制NLRP3炎性体途径降低促炎细胞因子的水平，从而抑制CAEC凋亡并保护冠心病大鼠的CAEC。 。

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