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首页> 外文期刊>RSC Advances >Curcumin alleviates LPS-induced inflammation and oxidative stress in mouse microglial BV2 cells by targeting miR-137-3p/NeuroD1
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Curcumin alleviates LPS-induced inflammation and oxidative stress in mouse microglial BV2 cells by targeting miR-137-3p/NeuroD1

机译：姜黄素通过靶向miR-137-3p / neurod1减轻小鼠小胶质Bv2细胞中的LPS诱导的炎症和氧化应激

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Curcumin has been reported to exert protective effects on inflammation-related diseases, including spinal cord injury (SCI). Numerous evidence have suggested miRNAs are one of the important targets for curcumin during its anti-inflammatory function. However, little is known about the contribution of miRNAs on the role of curcumin in SCI. Thus, the objective of this study is to determine the role of miRNA (miR)-137-3p during curcumin treatment after SCI. Expression of miR-137-3p and NeuroD1 was detected using RT-qPCR and western blot assay. Inflammation and oxidative stress were measured with the protein expression levels of tumor necrosis factor (TNF)-α, interleukin (IL)-1β, and inducible nitric oxide synthase (iNOS). The target binding between miR-137-3p and NeuroD1 was confirmed via the luciferase reporter assay and RNA immunoprecipitation. LPS induced a higher expression of TNF-α, IL-1β, and iNOS in mouse microglia BV2 cells, which was attenuated by curcumin. miR-137-3p was downregulated and NeuroD1 was upregulated under LPS challenge. Curcumin also alleviated LPS-induced regulation on miR-137-3p and NeuroD1. The knockdown of miR-137-3p and ectopic expression of NeuroD1 could individually abolish the curcumin-mediated downregulation of TNF-α, IL-1β, and iNOS in LPS-challenged BV2 cells. Besides, NeuroD1 was inversely regulated by miR-137-3p via direct binding. Silencing of NeuroD1 reversed the miR-137-3p downregulation-mediated promoting effect on inflammation and oxidative stress in the presence of LPS and curcumin. Downregulation of miR-137-3p abolishes curcumin-mediated protection on LPS-induced inflammation and oxidative stress in mouse microglial BV2 cells depending on the direct upregulation of NeuroD1.
机译：据报道，姜黄素对炎症相关的疾病产生保护作用，包括脊髓损伤（SCI）。许多证据表明MiRNA是抗炎功能期间姜黄素的重要靶标之一。然而，关于miRNA对姜黄素在SCI中的作用的贡献几乎是众所周知的。因此，本研究的目的是确定MiRNA（MIR）-137-3P在SCI后治疗期间miRNA（miR）-137-3p的作用。使用RT-QPCR和Western印迹测定检测miR-137-3p和neurod1的表达。用肿瘤坏死因子（TNF）-α，白细胞介素（IL）-1β和诱导型一氧化氮合酶（InOS）的蛋白表达水平测量炎症和氧化应激。通过荧光素酶报告酶测定和RNA免疫沉淀确认miR-137-3p和neurod1之间的靶结合。 LPS诱导小鼠微胶质细胞中的TNF-α，IL-1β和INOS的更高表达，所述小鼠小胶质细胞BV2细胞中的抗乳蛋白衰减。下调miR-137-3p，并且在LPS挑战下上调神经元1。姜黄素还缓解了LPS诱导的miR-137-3p和neurod1的调节。 MiR-137-3P的敲低和神经元的异位表达可以单独地消除LPS攻击的BV2细胞中TNF-α，IL-1β和InOS的姜黄素介导的下调。此外，Neurod1通过直接结合由miR-137-3p逆转。 Neurod1的沉默逆转MIR-137-3P在LPS和姜黄素存在下对炎症和氧化应激的促进促进作用。 MiR-137-3P的下调废除了姜黄素介导的对小鼠诱导的炎症和小鼠小鼠小鼠BV2细胞中的炎症和氧化应激的保护，这取决于神经元的直接上调。

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