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首页> 外文期刊>The Journal of toxicological sciences >COMMON PATHOGENIC MECHANISM IN DEVELOPMENT PROGRESSION OF LIVER INJURY CAUSED BY NON-ALCOHOLIC OR ALCOHOLIC STEATOHEPATITIS
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COMMON PATHOGENIC MECHANISM IN DEVELOPMENT PROGRESSION OF LIVER INJURY CAUSED BY NON-ALCOHOLIC OR ALCOHOLIC STEATOHEPATITIS

机译：非酒精性或酒精性脂肪性肝炎在肝损伤发展过程中的常见病原学机制

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This review showed the common pathogenic mechanism in the development of non-alcoholic or alcoholic steatohepatitis. In particular, we describe the role of innate immune system and oxida-tive stress caused by gut-derived endotoxin. Gut-derived endotoxin plays an important role in alcoholic liver injury. It was reported that acute ethanol administration reduced activation of Kupffer cells. It is therefore possible that alcohol-induced hepatocellular damage occurs as a result of bacterial or endotoxin translocation under a reduction of the reticuloendothelial system (RES) function in alcoholic liver disease (ALD). On the other hand, recently, attention has been directed toward the effect of ethanol ingestion on Kupffer cell function, which is stimulated by gut-derived endotoxin via mechanisms dependent on increased gut permeability and the possible relationship between Kupffer cells and alcohol-induced liver injury. It is generally accepted that activation of the innate immune system and increased release of proin-flammatory cytokines and other mediators plays an important role in the development of ALD. It was shown that Kupffer cells activation by endotoxin via Toll-like receptor (TLR-4) is involved in alcohol-induced liver injury and that ethanol-induced oxidative stress is important in the regulation of transcription factor NF-kB activation and that cytokine production by Kupffer cells. TNF-oc and free radicals are produced in early alcohol-induced liver injury. In support of this finding, the pathology caused by alcohol was blocked nearly completely in TNF-alpha receptor 1. Many pathways have been suggested to contribute to the ability of ethanol to induce a state of oxidative stress. One central pathway appears to be the induction of the CYP2E1 form of cytochrome P450 enzymes by ethanol. Initial efforts to clarify the mechanisms that promote the progression from steatosis to steatohepatitis somewhat artificially divides disease mechanisms into "first and second" hit. The best candidates for thesesecond hits were considered to be oxidative stress (CYP2E1 induction) and associated lipid peroxidation and cyokines, principally, TNF-alhpa. Some of the most definitive data on the importance of the innate immune system or oxidative stress in the pathogenesis of liver disease come from studies of alcoholic and non-alcoholic steatohepatitis in animals.
机译：这项审查显示了非酒精性或酒精性脂肪性肝炎发展的常见致病机制。特别是，我们描述了先天免疫系统和肠道源性内毒素引起的氧化应激的作用。肠源性内毒素在酒精性肝损伤中起重要作用。据报道，急性乙醇给药减少了库普弗细胞的活化。因此，在酒精性肝病（ALD）中网状内皮系统（RES）功能降低的情况下，细菌或内毒素易位是由于酒精引起的肝细胞损伤。另一方面，最近，注意力转向了乙醇摄入对库普弗细胞功能的影响，这种作用被肠源性内毒素通过依赖于肠通透性增加的机制以及库普弗细胞与酒精诱导的肝损伤之间可能的关系刺激而受到刺激。 。人们普遍认为，先天免疫系统的激活以及前炎症性细胞因子和其他介质的释放增加在ALD的发展中起着重要作用。研究表明，内啡肽通过Toll样受体（TLR-4）激活Kupffer细胞与酒精诱导的肝损伤有关，乙醇诱导的氧化应激在调节转录因子NF-kB激活和细胞因子产生中起重要作用。通过库普弗细胞。 TNF-α和自由基是在酒精引起的早期肝损伤中产生的。为了支持这一发现，由酒精引起的病理几乎完全被TNF-α受体1阻断。已提出许多途径有助于乙醇诱导氧化应激状态。一个主要途径似乎是乙醇诱导CYP2E1形式的细胞色素P450酶。为弄清促进从脂肪变性发展为脂肪性肝炎的机制所做的初步努力在某种程度上是人为地将疾病机制分为“第一和第二”。这些第二次命中的最佳候选者被认为是氧化应激（CYP2E1诱导）以及相关的脂质过氧化和趋化因子，主要是TNF-alhpa。关于先天免疫系统或氧化应激在肝病发病机制中重要性的一些最权威的数据来自动物酒精性和非酒精性脂肪性肝炎的研究。

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