姜黄素通过调节 miR-362-3p/TLR4 轴保护 BV2 细胞免受脂多糖诱导的损伤。
Curcumin protects BV2 cells against lipopolysaccharide-induced injury via adjusting the miR-362-3p/TLR4 axis.
机构信息
Department of Chinese Traditional Medicine, TongRen Hospital of Wuhan University (Wuhan Third Hospital), Wuhan, Hubei, China.
Department of Orthopedics, Renmin Hospital of Wuhan University, No. 238, Jiefang Road, Wuhan, 430060, Hubei, China.
出版信息
Mol Biol Rep. 2020 Jun;47(6):4199-4208. doi: 10.1007/s11033-020-05543-y. Epub 2020 May 29.
Curcumin was demonstrated to be an active ingredient with anti-inflammatory effects. This research was to investigate the effects of curcumin. We found that curcumin promoted cell viability and suppressed cell apoptosis. Meanwhile, curcumin decreased the level of cleaved caspase-3 and the release of TNF-α, IL-1β, IL-6, but increased IL-10 release in LPS-treated BV2 cells. miR-362-3p expression was upregulated by curcumin, while TLR4 expression was downregulated. Besides, we observed that the cytoprotective effects of curcumin were lost when miR-362-3p was silenced. TLR4 was a direct target gene of miR-362-3p. Moreover, miR-362-3p deletion attenuated the cytoprotective effects of curcumin by regulating TLR4 expression in LPS-induced BV2 cells. Furthermore, curcumin suppressed p-p65 expression via regulating miR-362-3p/TLR4 axis. We discovered that curcumin exhibited protective effects against LPS-triggered cell injury via modulating miR-362-3p/TLR4 axis through NF-κB pathway.
姜黄素被证实是一种具有抗炎作用的活性成分。本研究旨在探讨姜黄素的作用。我们发现姜黄素促进细胞活力，抑制细胞凋亡。同时，姜黄素降低了 LPS 处理的 BV2 细胞中 cleaved caspase-3 和 TNF-α、IL-1β、IL-6 的释放水平，但增加了 IL-10 的释放。姜黄素上调了 miR-362-3p 的表达，同时下调了 TLR4 的表达。此外，当 miR-362-3p 被沉默时，姜黄素的细胞保护作用消失了。TLR4 是 miR-362-3p 的直接靶基因。此外，miR-362-3p 缺失通过调节 TLR4 表达减弱了姜黄素对 LPS 诱导的 BV2 细胞的保护作用。此外，姜黄素通过调节 miR-362-3p/TLR4 轴抑制 p-p65 的表达。我们发现姜黄素通过 NF-κB 通路调节 miR-362-3p/TLR4 轴，对 LPS 触发的细胞损伤表现出保护作用。
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