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根据是否饮酒和饮酒量的多少将脂防肝分为酒精性和非酒精性。乙醇及其代谢产物可对肝细胞、炎症细胞、肝星状细胞等起引发和致敏性损伤。乙醇诱致氧应激、内毒素及细胞因子产生失调,通过细胞内和细胞间的信号级联反应介导并放大组织损伤。参与信号级联反应的小分子物质(如细胞内Ca2+)、应激活化的蛋白激酶、转录因子、凋亡信号调节物等,通过不同的信号通道发挥其生物化学效应。
According to whether the amount of alcohol consumption and alcohol will be divided into lipid and non-alcoholic liver. Ethanol and its metabolites can cause priming and sensitization damage to hepatocytes, inflammatory cells and hepatic stellate cells. Ethanol induces the imbalance of oxygen stress, endotoxin and cytokines, and mediates and amplifies the tissue damage through intracellular and intercellular signaling cascades. Small molecules (such as intracellular Ca2 +), stress-activated protein kinases, transcription factors and apoptotic signal regulators involved in signal cascade reactions exert their biochemical effects through different signaling pathways.