Suppr超能文献

姜黄素通过抑制 NF-κB 和 JNK 信号通路缓解脂多糖诱导的血管平滑肌细胞炎症和凋亡。

Curcumin alleviates lipopolysaccharides-induced inflammation and apoptosis in vascular smooth muscle cells via inhibition of the NF-κB and JNK signaling pathways.

机构信息

Department of Cardiology, Jiangxi Provincial People's Hospital, Nanchang, 330000, Jiangxi, People's Republic of China.

School of Software and Internet of Things Engineering, Jiangxi University of Finance and Economics, Nanchang, Jiangxi, People's Republic of China.

出版信息

Inflammopharmacology. 2022 Apr;30(2):517-525. doi: 10.1007/s10787-021-00912-w. Epub 2022 Mar 1.

Abstract

Curcumin plays an important role in inflammation regulation. This study aimed to investigate the effect of curcumin on vascular smooth muscle cells (VSMCs) inflammation induced by lipopolysaccharide (LPS) and its mechanism. VSMCs were treated with different concentrations of curcumin (0, 50, 100 and 150 μg/mL). MTT assay and flow cytometry were used to analyze the effects of curcumin on LPS-induced VSMCs viability and apoptosis. The expression and release of inflammatory cytokines in VSMCs were detected by real-time quantitative polymerase chain reaction (qRT-PCR) and enzyme-linked immunosorbent assay (ELISA). Moreover, the proteins expressions of NF-κB and JNK signaling pathways were analyzed by western blot. Interestingly, the results showed that curcumin could reduce LPS induced inflammatory injury by increasing VSMC's viability, reducing apoptosis and inhibiting the release of inflammatory cytokines. In addition, curcumin increased the expression of Toll-like receptor 4 (TLR4) in LPS treated VSMCs. Mechanistically, we found that curcumin attenuated LPS-induced cell damage in VSMCs via inhibition of NF-κB and the JNK signal pathway. Curcumin can protect VSMCs from LPS induced inflammatory damage, which may be related to the blocking of NF-κB and the JNK signaling pathway. Herewith, curcumin could be potential therapeutics for the treatment of atherosclerosis.

摘要

姜黄素在炎症调节中发挥着重要作用。本研究旨在探讨姜黄素对脂多糖(LPS)诱导的血管平滑肌细胞(VSMCs)炎症的影响及其机制。用不同浓度的姜黄素(0、50、100 和 150μg/mL)处理 VSMCs。MTT 法和流式细胞术分析姜黄素对 LPS 诱导的 VSMCs 活力和凋亡的影响。实时定量聚合酶链反应(qRT-PCR)和酶联免疫吸附试验(ELISA)检测 VSMCs 中炎症细胞因子的表达和释放。此外,通过 Western blot 分析 NF-κB 和 JNK 信号通路的蛋白表达。有趣的是,结果表明姜黄素通过增加 VSMC 的活力、减少凋亡和抑制炎症细胞因子的释放,减轻 LPS 诱导的炎症损伤。此外,姜黄素增加了 LPS 处理的 VSMCs 中 Toll 样受体 4(TLR4)的表达。在机制上,我们发现姜黄素通过抑制 NF-κB 和 JNK 信号通路来减轻 LPS 诱导的 VSMCs 细胞损伤。姜黄素可以保护 VSMCs 免受 LPS 诱导的炎症损伤,这可能与阻断 NF-κB 和 JNK 信号通路有关。因此,姜黄素可能是治疗动脉粥样硬化的潜在治疗方法。

文献AI研究员

20分钟写一篇综述,助力文献阅读效率提升50倍。

立即体验

用中文搜PubMed

大模型驱动的PubMed中文搜索引擎

马上搜索

文档翻译

学术文献翻译模型,支持多种主流文档格式。

立即体验