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首页> 外文期刊>Cellular Physiology and Biochemistry >Ischemia and Reperfusion Liver Injury is Reduced in the Absence of Toll-like Receptor 4
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Ischemia and Reperfusion Liver Injury is Reduced in the Absence of Toll-like Receptor 4

机译：缺乏Toll样受体4可以减少缺血和再灌注肝损伤

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biBackground/Aims /i/bToll-like receptor 4 (TLR4) is expressed on hepatic non-parenchymal cells and hepatocytes. Hepatic signaling through TLR4 is critical in the pathogenesis of ischemia reperfusion injury (IRI) and leads to the release of cytokines. The role of bone marrow-derived TLR4 in the early reperfusion stage is unclear. biMethods /i/bWe used wild type mice (WT), TLR4deficient (TLR4ko) mice and chimeras to dissociate between the role of TLR4 expression in the liver (TLR4ko/WT) and in the immuno-hematopoietic system (WT/TLR4ko) in mouse hepatic IR injury model. Mice were subjected to iin vivo /ipartial IRI (70% for 60 min). biResults /i/bCompared with WT IR livers, TLR4ko IRI mice (4 hours) showed a significant reduction in serum liver enzyme, hepatic TNF-α and interleukin-1β levels. Fewer apoptotic hepatocytes cells were identified by morphological criteria and immunohistochemistry for caspase-3. In TLR4ko mice, decreased hepatic CJUN and NF-?B expression during IRI was noted compared with WT mice. Chimeric mice having either TLR4 bone-marrow or non-bone marrow derived cells following IRI exhibited almost similar hepatic injury as WT mice in the immediate reperfusion stage. biConclusion /i/bBoth TLR4 bone marrow-derived and non-bone marrow-derived cells are necessary in the initial process of hepatic injury. Activating TLR4-dependent signaling is required for IRI. The absence of the TLR4 gene plays a pivotal role in reducing hepatic IR injury.
机译：背景/目的 Toll样受体4（TLR4）在肝非实质细胞和肝细胞上表达。通过TLR4传递的肝信号在缺血再灌注损伤（IRI）的发病机理中至关重要，并导致细胞因子的释放。骨髓TLR4在早期再灌注阶段的作用尚不清楚。 方法 我们使用野生型小鼠（WT），TLR4缺陷（TLR4ko）小鼠和嵌合体来分离TLR4表达在肝脏（TLR4ko / WT）和肝细胞中的作用。小鼠肝脏IR损伤模型中的免疫造血系统（WT / TLR4ko）。对小鼠进行体内部分IRI（70％，持续60分钟）。 结果 与WT IR肝脏相比，TLR4ko IRI小鼠（4小时）显示血清肝酶，肝TNF-α和白介素1β的水平明显降低。通过形态学标准和caspase-3的免疫组织化学鉴定出较少的凋亡肝细胞。与野生型小鼠相比，在TLR4ko小鼠中，IRI期间肝脏CJUN和NF-κB表达降低。 IRI后具有TLR4骨髓或非骨髓来源细胞的嵌合小鼠在立即再灌注阶段表现出与WT小鼠几乎相似的肝损伤。 结论 在肝损伤的初始过程中，TLR4骨髓来源的细胞和非骨髓来源的细胞都是必需的。 IRI需要激活TLR4依赖的信令。 TLR4基因的缺失在减少肝IR损伤中起关键作用。

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