川芎嗪抑制NF-κB P65磷酸化对LPS诱导的骨关节炎软骨细胞凋亡和炎症反应的调节作用

被引：61

作者：

朱海泉 ^{[1
]}

刘子敏 ^{[1
]}

孟祥圣 ^{[1
]}

孙晓 ^{[1
]}

王黎明 ^{[2
]}

机构：

[1] 南京医科大学连云港临床医学院急诊外科

[2] 南京医科大学附属南京医院骨科

来源：

中国免疫学杂志 | 2019年 / 35卷 / 02期

关键词：

川芎嗪; 骨关节炎; 细胞凋亡; 炎症; NF-κB P65;

D O I：

暂无

中图分类号：

R684.3 [关节炎];

学科分类号：

100220 [骨科学];

摘要：

目的:探讨川芎嗪对LPS诱导的骨关节炎软骨细胞凋亡和炎症反应的影响及机制。方法:LPS诱导骨关节炎模型。软骨细胞分为4个组:对照组;川芎嗪(20μmol/L)组; LPS(100 ng/ml)组;川芎嗪(20μmol/L)+LPS(100 ng/ml)组。Hoechst33258染色检测细胞凋亡。ELISA检测一氧化氮(Nitric oxide,NO)、肿瘤坏死因子-α(TNF-α)和白细胞介素(IL)-6水平。蛋白印迹检测Ⅱ型胶原(collagenⅡ)、聚集蛋白聚糖(aggrecan)和基质金属蛋白酶-13(MMP-13)、NF-κB P65和p-NF-κB P65蛋白水平。结果:川芎嗪(20μmol/L)可改善LPS诱导的骨关节炎软骨细胞形态异常及细胞数量的减少。LPS组细胞凋亡率明显高于对照组(P<0. 05)。川芎嗪可降低LPS诱导的细胞凋亡率的升高(P<0. 05)。与对照组相比,LPS组Ⅱ型胶原和聚集蛋白聚糖表达明显降低,MMP-13表达明显升高(P<0. 05)。川芎嗪可抑制LPS诱导的Ⅱ型胶原和聚集蛋白聚糖表达水平的下降及MMP-13表达水平的上升(P<0. 05)。LPS组NO、TNF-α和IL-6水平明显高于对照组(P<0. 05)。LPS+川芎嗪组NO、TNF-α和IL-6水平显著低于LPS组(P<0. 05)。与对照组相比,LPS组p-P65/P65比值明显升高(P<0. 05)。川芎嗪可减弱LPS诱导的p-P65/P65比值的上升(P<0. 05)。结论:川芎嗪通过抑制NF-κB P65磷酸化减轻LPS诱导的骨关节炎软骨细胞凋亡和炎症反应。

引用

页码：181 / 185

页数：5

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