通过抑制血管平滑肌细胞(VSMCs)中由 NF-κB/NLRP3/IL-1β 通路介导的嗜热症来减轻动脉粥样硬化

IF 3.4 4区 医学 Q2 CARDIAC & CARDIOVASCULAR SYSTEMS
Shihuan Li, Qingjie Li, Qiaofeng Zhou, Suqin Li, Siqi Wang, Qing Yao, Changhan Ouyang, Chao Liu, Mincai Li
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引用次数: 0

摘要

研究目的研究白藜芦醇(Res)和 MCC950 对血管平滑肌细胞(VSMCs)热休克的影响及其潜在途径。方法和结果。与对照(Con)组相比,动脉粥样硬化(AS)组出现了钙化结节,这表明钙化介质诱导了 VSMC 的钙化。在 10 μmol/L Res 的作用下,VSMCs 表现出增殖活性,并明显减轻了钙化。通过RT-qPCR、Western印迹和免疫荧光,Res和MCC950下调了钙化、炎症、热休克和转录因子相关指标。结果表明,Res和MCC950均能抑制VSMC的钙化,且Res的效果优于MCC950。对照组颈动脉区域存在斑块和钙盐沉积。通过 HE 染色和茜素红 S 染色,Par 组的斑块中有更多的钙盐沉积。免疫荧光显示,钙化指标BMP2、Runx2及相关指标下降,这表明parthenolide抑制了AS。相关蛋白表达与细胞实验表达一致。结论我们的数据表明,炎症反应和脓毒症会加重强直性脊柱炎,并揭示了 VSMC 与强直性脊柱炎病变进展之间的联系。Res和MCC950通过调节NF-κB/NLRP3/IL-1β信号轴抑制了VSMCs的钙化。P53可通过作用于NLRP3炎症小体和脓毒血症而加重强直性脊柱炎的病变。我们的研究结果支持了Res和MCC950在VSMCs个体中的临床应用,以对抗热蛋白沉积和强直性脊柱炎,P53抑制剂也是治疗强直性脊柱炎的一种潜在方法。
本文章由计算机程序翻译,如有差异,请以英文原文为准。
Attenuating Atherosclerosis through Inhibition of the NF-κB/NLRP3/IL-1β Pathway-Mediated Pyroptosis in Vascular Smooth Muscle Cells (VSMCs)

Objective. We investigated the effects of resveratrol (Res) and MCC950 on the pyroptosis of vascular smooth muscle cells (VSMCs) and the potential pathway. Methods and Results. Compared with the control (Con) group, the atherosclerosis (AS) group showed calcified nodules, which suggested that the calcification medium induced the calcification of VSMCs. VSMCs showed proliferative activity and significantly attenuated calcification under treatment with 10 μmol/L Res. The calcium salt was detected by alizarin red S staining. Res and MCC950 downregulated the calcification, inflammatory, pyroptosis, and transcription factor-related indicators all decreased by RT-qPCR with Western blot and immunofluorescence. The results showed that Res and MCC950 refrained the calcification of VSMCs and that Res has a better effect than MCC950. Plaques and calcium salt deposits were present in the carotid region in the control group. More calcium salt deposits were evident in the plaques of the Par group by HE staining and alizarin red S staining. The calcification indexes BMP2, Runx2, and related indexes declined by immunofluorescence, which showed parthenolide-inhibited AS. The related protein expressions were consistent with the expression of the cell experiments. Conclusion. Our data demonstrated that inflammatory response and pyroptosis exacerbate AS and unravel the link between VSMCs and the progression of AS lesions. Res and MCC950 inhibited the calcification of VSMCs by regulating NF-κB/NLRP3/IL-1β signaling axis. P53 can exacerbate the AS lesions by acting on NLRP3 inflammasome and pyroptosis. Our findings supported the clinical applications of Res and MCC950 in VSMCs individuals to counteract pyroptosis and AS, and P53 inhibitors also can be a potential treatment for AS.

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来源期刊
Cardiovascular Therapeutics
Cardiovascular Therapeutics 医学-心血管系统
CiteScore
5.60
自引率
0.00%
发文量
55
审稿时长
6 months
期刊介绍: Cardiovascular Therapeutics (formerly Cardiovascular Drug Reviews) is a peer-reviewed, Open Access journal that publishes original research and review articles focusing on cardiovascular and clinical pharmacology, as well as clinical trials of new cardiovascular therapies. Articles on translational research, pharmacogenomics and personalized medicine, device, gene and cell therapies, and pharmacoepidemiology are also encouraged. Subject areas include (but are by no means limited to): Acute coronary syndrome Arrhythmias Atherosclerosis Basic cardiac electrophysiology Cardiac catheterization Cardiac remodeling Coagulation and thrombosis Diabetic cardiovascular disease Heart failure (systolic HF, HFrEF, diastolic HF, HFpEF) Hyperlipidemia Hypertension Ischemic heart disease Vascular biology Ventricular assist devices Molecular cardio-biology Myocardial regeneration Lipoprotein metabolism Radial artery access Percutaneous coronary intervention Transcatheter aortic and mitral valve replacement.
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