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蛹虫草多糖抑制血小板衍生生长因子 BB 诱导的人肾小球系膜细胞炎症和 ROS 产生。

Cordyceps sinensis polysaccharide inhibits PDGF-BB-induced inflammation and ROS production in human mesangial cells.

机构信息

State Key Laboratory of Natural Medicines, China Pharmaceutical University, Nanjing 210009, People's Republic of China; School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, Jiangsu, People's Republic of China.

School of Life Science and Technology, China Pharmaceutical University, Nanjing 210009, Jiangsu, People's Republic of China.

出版信息

Carbohydr Polym. 2015 Jul 10;125:135-45. doi: 10.1016/j.carbpol.2015.02.012. Epub 2015 Feb 19.

Abstract

CPS-F, a polysaccharide derived from Cordyceps sinensis, is a potential anti-inflammatory and anti-oxidative agent. We demonstrated that CPS-F not only inhibits platelet-derived growth factor BB (PDGF-BB)-induced intracellular reactive oxygen species (ROS) generation, and up-regulation of tumor necrosis factor-α (TNF-α), TNF-α receptor 1 (TNFR1), and monocyte chemotactic protein-1 (MCP-1), but also acts synergistically in combination with MAPK/ERK inhibitor U0126 and PI3K/Akt inhibitor LY294002. Additionally, up-regulation of pro-inflammatory factors was reversed by use of a combination of CPS-F and NADPH oxidase (NOX) inhibitor diphenyleneiodonium chloride (DPI) or silencing of NOX1. Furthermore, CPS-F prevents the PDGF receptor β (PDGFRβ) promoter activity induced by PDGF-BB in transfected cells and ameliorates increased levels of TNF-α, TNFR1, and MCP-1 when PDGFRβ is silenced, thereby suggesting that CPS-F possesses a bidirectional regulatory function. Our findings suggest CPS-F may exert its therapeutic effect for the treatment of glomerulonephritis related to human mesangial cells (HMCs) through the ERK1/2/Akt pathways.

摘要

CPS-F,一种源自冬虫夏草的多糖,是一种有潜力的抗炎和抗氧化剂。我们证明 CPS-F 不仅能抑制血小板衍生生长因子 BB(PDGF-BB)诱导的细胞内活性氧(ROS)生成,以及肿瘤坏死因子-α(TNF-α)、TNF-α 受体 1(TNFR1)和单核细胞趋化蛋白-1(MCP-1)的上调,而且与 MAPK/ERK 抑制剂 U0126 和 PI3K/Akt 抑制剂 LY294002 联合使用还具有协同作用。此外,使用 NADPH 氧化酶(NOX)抑制剂二苯基碘(DPI)或沉默 NOX1,上调促炎因子的作用得到逆转。此外,CPS-F 可防止 PDGF-BB 在转染细胞中诱导 PDGF 受体β(PDGFRβ)启动子活性,并减轻 PDGFRβ 沉默时 TNF-α、TNFR1 和 MCP-1 水平的升高,这表明 CPS-F 具有双向调节功能。我们的研究结果表明,CPS-F 可能通过 ERK1/2/Akt 通路发挥其治疗肾小球肾炎相关人系膜细胞(HMC)的作用。

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