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柚皮苷抑制脂多糖诱导的小胶质细胞活化。

Naringin inhibits lipopolysaccharide-induced activation of microglia cells.

作者信息

Bai Jie, Li Siyuan, Wu Gang, Ma Lei, Li Chen, Liu Hongtao, Zhang Pengbo

机构信息

Department of Anesthesiology, the Second Affiliated Hospital of Xi'an Jiaotong University, 710004, Xi'an, Shaanxi, China.

Department of Geriatrics Neurology, the Second Affiliated Hospital of Xi'an Jiaotong University, No. 157 Xiwu Road, 710004, Xi'an, Shaanxi, China.

出版信息

Cell Mol Biol (Noisy-le-grand). 2019 Jun 30;65(5):38-42.

Abstract

The purpose of this study was to investigate the effect of naringin on lipopolysaccharide (LPS)-induced activation of BV2 microglia and inflammatory factor release, and the mechanism involved. Different concentrations of naringin were used to pretreat BV2 cells for 30 min, after which they were stimulated with 100 ng/mL LPS for different durations. The levels of NO, IL-1β and TNF-α in the cell culture medium was determined with ELISA and Griess method. The mRNA expressions of IL-1β and TNF-α was determined with RT-PCR. Changes in ERK and p65/NF-κB signaling pathway proteins were assayed with Western blotting. After 12 h stimulation of BV2 cells with LPS, the levels of IL-1β and TNF-α in the cell culture medium were significantly increased, but naringin had no significant effect on these inflammatory factors. In the cells pretreated with naringin, LPS stimulated the activation of microglia to produce IL-1β and TNF-α in a dose-dependent manner. Naringin inhibited LPS-induced release of IL-1β, to a certain extent. The TNF-α gene was overexpressed. In addition, LPS stimulated a dose-dependent decrease in NO production by BV2 after pretreatment with different concentrations of naringin. Naringin pretreatment of cells significantly inhibited the activation of p65/NF-κB in a concentration-dependent manner. In BV2 microglia, naringin inhibits LPO-induced production of NO and inflammatory factors, through a mechanism involving inhibition of activation of the p65/NF-κB signaling pathway.

摘要

本研究旨在探讨柚皮苷对脂多糖(LPS)诱导的BV2小胶质细胞活化及炎性因子释放的影响及其作用机制。采用不同浓度的柚皮苷预处理BV2细胞30分钟,之后用100 ng/mL LPS刺激不同时长。用ELISA和Griess法测定细胞培养基中NO、IL-1β和TNF-α的水平。用RT-PCR测定IL-1β和TNF-α的mRNA表达。用蛋白质印迹法检测ERK和p65/NF-κB信号通路蛋白的变化。用LPS刺激BV2细胞12小时后,细胞培养基中IL-1β和TNF-α的水平显著升高,但柚皮苷对这些炎性因子无显著影响。在用柚皮苷预处理的细胞中,LPS以剂量依赖性方式刺激小胶质细胞活化产生IL-1β和TNF-α。柚皮苷在一定程度上抑制LPS诱导的IL-1β释放。TNF-α基因过表达。此外,用不同浓度柚皮苷预处理后,LPS刺激BV2产生NO的量呈剂量依赖性降低。用柚皮苷预处理细胞可显著抑制p65/NF-κB的活化,且呈浓度依赖性。在BV2小胶质细胞中,柚皮苷通过抑制p65/NF-κB信号通路的活化机制,抑制LPO诱导的NO和炎性因子的产生。

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