| 脂多糖通过MAPK信号通路诱导肾小管上皮细胞核因子κB抑制蛋白释放 |
| 投稿时间：2015-07-13 修订日期：2015-08-02 点此下载全文 |
| 引用本文：吴乙偲,郑世翔,陈星华,丁国华.脂多糖通过MAPK信号通路诱导肾小管上皮细胞核因子κB抑制蛋白释放[J].医学研究杂志,2016,45(2):47-50 |
| DOI：
10.11969/j.issn.1673-548X.2016.02.013 |
| 摘要点击次数: 1998 |
| 全文下载次数: 1015 |
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| 基金项目:国家自然科学基金资助项目(81070556);湖北省自然科学基金资助项目(2015CFB347) |
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| 中文摘要:目的 观察脂多糖(LPS)刺激肾小管上皮细胞(NRK-52E)后核因子κB抑制蛋白(I-κB)的表达,分析MAPK信号通路的变化与I-κB的关联,探讨LPS促进NRK-52E细胞炎性反应的信号通路的变化。方法 细胞同步化后,将其分为对照组、LPS(1μg/ml)组、MAPK抑制剂组,LPS刺激不同时间(5、15、30、60min)后免疫印迹法检测p38、JNK MAPK及I-κB磷酸化水平,给予抑制剂6h后免疫印迹法检测I-κB磷酸化水平。结果 与对照组相比,LPS显著上调NRK-52E细胞p38、JNK MAPK及I-κB磷酸化水平(P均<0.05)。与LPS组相比,MAPK抑制剂干预显著抑制LPS诱导的细胞I-κB的释放(P<0.05)。结论 LPS对NRK-52E细胞MAPK信号通路具有激活效应,该信号通路激活可能是LPS促进肾小管上皮细胞炎性相关因子释放的重要机制之一。 |
| 中文关键词:脂多糖 肾小管上皮细胞 MAPK信号通路 炎性因子 |
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| Abstract:Objective To observe the release of inflammatory factors after lipopolysaccharide stimulation in renal tubular epithelial cells(NRK-52E), to analyze whether the effects were mediated by MAPK signalling pathway, and to reveal the mechanism of injury by LPS on NRK-52E cells. Methods After synchronization, cells incubated with LPS(1μg/ml) were used as the stimulation groups, cells without stimulation were as normal control. To determine the role of MAPK signalling pathway, equal number of NRK-52E cells was added with MAPK signalling pathway inhibitors for 6 h and then incubated with LPS(1μg/ml).Western blot was used to analyze the phosphorylation of p38, JNK, I-κB expression. Results The phosphorylation of p38, JNK were highly expressed in LPS-induced NRK-52E cells(P<0.05), and the I-κB level were also increased markedly compared with control group(P<0.05). In NRK-52E cells that were pre-incubated with MAPK signalling pathway inhibitors, the phosphorylation of I-κB were obviously inhibited compared with LPS group(P<0.05). Conclusion The mechanism of LPS-induced injury effect on NRK-52E cells is related to the phosphorylation of p38, JNK MAPK signalling pathway, which is followed by the enhance ment of the phosphorylation of I-κB expression. This process is inhibited by MAPK signalling pathway inhibitor via modulation of inflammation pathway. |
| keywords:Lipopolysaccharide Renal tubular epithelial cells(NRK-52E) MAPK signalling pathway Inflammatory factor |
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