Down-Regulated Receptor Interacting Protein 140 Is Involved in Lipopolysaccharide-Preconditioning-Induced Inactivation of Kupffer Cells and Attenuation of Hepatic Ischemia Reperfusion Injury.
Down-Regulated Receptor Interacting Protein 140 Is Involved in Lipopolysaccharide-Preconditioning-Induced Inactivation of Kupffer Cells and Attenuation of Hepatic Ischemia Reperfusion Injury.
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下调受体相互作用蛋白 140 参与脂多糖预处理诱导的枯否细胞失活和肝缺血再灌注损伤的减轻
DOI：
10.1371/journal.pone.0164217
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发表时间：
2016
期刊：
影响因子：
3.7
通讯作者：
Zuojin L
中科院分区：
文献类型：
--
作者：
Yuan G;Yu Y;Ji L;Jie X;Yue L;Kang Y;Jianping G;Zuojin L
已知脂多糖（LPS）预处理可减轻肝脏缺血/再灌注损伤（I/RI）；然而，其确切机制仍不清楚。本研究探讨了受体相互作用蛋白140（RIP140）在LPS预处理对涉及枯否细胞（KCs）的肝脏I/RI的保护作用中的角色。
斯普拉格 - 道利大鼠经历70%肝脏缺血90分钟。在缺血前24小时腹腔注射LPS（100μg/kg）。利用血清和肝脏样本观察肝脏损伤。研究了分离的枯否细胞中的LPS/NF - κB（核因子 - κB）通路和肝脏RIP140表达。
LPS预处理显著抑制了I/RI后的肝脏RIP140表达、NF - κB活化以及血清促炎细胞因子表达，同时观察到血清酶水平和组织病理学评分显著降低。我们的实验表明，LPS预处理可在枯否细胞中有效诱导保护作用，但当枯否细胞中RIP140过表达时则不能。相反，即使没有LPS预处理，如果用小干扰RNA抑制RIP140表达，在枯否细胞中也能发现保护作用。
RIP140下调参与了LPS诱导的枯否细胞失活以及肝脏I/RI的减轻。
Background Lipopolysaccharide (LPS) preconditioning is known to attenuate hepatic ischemia/reperfusion injury (I/RI); however, the precise mechanism remains unclear. This study investigated the role of receptor-interacting protein 140 (RIP140) on the protective effect of LPS preconditioning in hepatic I/RI involving Kupffer cells (KCs). Methods Sprague—Dawley rats underwent 70% hepatic ischemia for 90 minutes. LPS (100 μg/kg) was injected intraperitoneally 24 hours before ischemia. Hepatic injury was observed using serum and liver samples. The LPS/NF-κB (nuclear factor-κB) pathway and hepatic RIP140 expression in isolated KCs were investigated. Results LPS preconditioning significantly inhibited hepatic RIP140 expression, NF-κB activation, and serum proinflammatory cytokine expression after I/RI, with an observation of remarkably reduced serum enzyme levels and histopathologic scores. Our experiments showed that protection effects could be effectively induced in KCs by LPS preconditioning, but couldn’t when RIP140 was overexpressed in KCs. Conversely, even without LPS preconditioning, protective effects were found in KCs if RIP140 expression was suppressed with siRNA. Conclusions Down-regulated RIP140 is involved in LPS-induced inactivation of KCs and hepatic I/RI attenuation.
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DOI：
10.1186/cc13110
发表时间：
2013-11-14
期刊：
Critical care (London, England)
影响因子：
--
作者：
López-Collazo E;del Fresno C
通讯作者：
del Fresno C
影响因子：
--
作者：
Vasilescu C;Olteanu M;Flondor P;Calin GA
通讯作者：
Calin GA
脂多糖预处理通过抑制小鼠 ATF4-CHOP 通路来保护肝细胞免受缺血/再灌注损伤 (IRI)。
影响因子：
3.7
作者：
Rao J;Qin J;Qian X;Lu L;Wang P;Wu Z;Zhai Y;Zhang F;Li G;Wang X
通讯作者：
Wang X
影响因子：
8.8
作者：
Rao, J.;Qian, X.;Lu, L.
通讯作者：
Lu, L.
影响因子：
13.5
作者：
Ji, Haofeng;Liu, Yuanxing;Zhang, Yu;Shen, Xiu-da;Gao, Feng;Busuttil, Ronald W.;Kuchroo, Vijay K.;Kupiec-Weglinski, Jerzy W.
通讯作者：
Kupiec-Weglinski, Jerzy W.