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

被引：4

作者：

吴乙偲

郑世翔

陈星华

丁国华

机构：

[1] 武汉大学人民医院肾内科

来源：

医学研究杂志 | 2016年 / 45卷 / 02期

关键词：

脂多糖; 肾小管上皮细胞; MAPK信号通路; 炎性因子;

D O I：

暂无

中图分类号：

R692 [肾疾病];

学科分类号：

100221 [泌尿外科学];

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。

引用

页码：47 / 50

页数：4

共 9 条

[1]

Cilostazol inhibits HMGB1 release in LPS-activated RAW 264.7 cells and increases the survival of septic mice [J].

Chang, Ki Churl .

THROMBOSIS RESEARCH, 2015, 136 (02) :456-464

[2]

c-Jun N -terminal kinase inhibitors: a patent review (2010 – 2014).[J].Matthias Gehringer;Felix Muth;Pierre Koch;Stefan A Laufer.Expert Opinion on Therapeutic Patents.2015, 8

[3]

The problem of pyridinyl imidazole class inhibitors of MAPK14/p38α and MAPK11/p38β in autophagy research [J].

Menon, Manoj B. ;

Dhamija, Sonam ;

Kotlyarov, Alexey ;

Gaestel, Matthias .

AUTOPHAGY, 2015, 11 (08) :1425-1427

[4]

CD200R1 agonist attenuates LPS-induced inflammatory response in human renal proximal tubular epithelial cells by regulating TLR4-MyD88-TAK1-mediated NF-κB and MAPK pathway [J].

Ding, Yan ;

Yang, Huilan ;

Xiang, Wei ;

He, Xiaojie ;

Liao, Wang ;

Yi, Zhuwen .

BIOCHEMICAL AND BIOPHYSICAL RESEARCH COMMUNICATIONS, 2015, 460 (02) :287-294

[5]

Role of TLR4 in lipopolysaccharide-induced acute kidney injury: Protection by blueberry.[J].Anand R. Nair;Gustavo S. Masson;Philip J. Ebenezer;Fabio Del Piero;Joseph Francis.Free Radical Biology and Medicine.2014,

[6]

Gram-positive and gram-negative bacterial toxins in sepsis.[J].Girish Ramachandran.Virulence.2014, 1

[7]

Signalling mechanisms involved in renal pathological changes during cisplatin-induced nephropathy [J].