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肝纤维化是慢性肝脏疾病的重要病理特征,主要由于肝脏细胞外基质代谢失衡,合成超过降解所致,肝纤维化和原代细胞培养的早期,肝星状细胞(HSC)短暂表达基质金属蛋白酶-3(MMP-3)、MMP-13和尿激酶型纤溶酶原激活物(uPA)并表现为降解基质的表型,肝纤维化进展期和HSC培养的晚期,HSC可表达降解正常肝基质,但抑制肝纤维化中沉积的胶原纤维降解的MMPs成分,同时金属蛋白酶组织抑制物(TIMPs)的表达增加,抑制MMPs的活性,肝纤维化恢复期TIMPs迅速下凋,MMPs活性增加。肝基质降解,导致肝纤维化消退。
Liver fibrosis is an important pathological feature of chronic liver disease, mainly due to imbalance of extracellular matrix metabolism in the liver, synthesis of more than the degradation caused by liver fibrosis and early primary cell culture, hepatic stellate cells (HSC) transiently express matrix metalloproteinase -3 (MMP-3), MMP-13, and urokinase-type plasminogen activator (uPA) and display a phenotype of degradative matrix, progression of liver fibrosis and late HSC culture, HSCs express degradable normal liver Matrix, but inhibited the degradation of MMPs by collagen fibers deposited in hepatic fibrosis. At the same time, the expression of tissue inhibitors of metalloproteinases (TIMPs) increased and the activity of MMPs was inhibited. The TIMPs rapidly wilted and the activity of MMPs increased during the recovery of liver fibrosis. Liver matrix degradation, leading to regression of liver fibrosis.