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目的:观察甘草酸二铵抗大鼠实验性肝纤维化的作用效果并探讨其作用机制。方法:采用二甲基亚硝胺诱导的大鼠肝纤维化模型,以高剂量(60 gmg/kg)和低剂量(15 mg/kg)的甘草酸二铵进行干预治疗,并与秋水仙碱进行对照,检测大鼠肝功能、肝组织羟脯胺酸(Hyp)、丙二醛(MDA)、血清透明质酸(HA)和层粘连蛋白(LN)含量变化,观察肝组织病理学改变和基质金属蛋白酶2(MMP-2)表达。结果:甘草酸二铵高、低剂量组大鼠血清丙氨酸氨基转移酶(ALT)、门冬氨酸氨基转移酶(AST)、碱性磷酸酶(ALP)、总胆红素(TBIL)水平均显著低于模型组(P<0.01)。甘草酸二铵高剂量组大鼠肝组织Hyp、MDA、血清HA和LN含量均显著低于模型组(P<0.01),与秋水仙碱组比较差异显著(P<0.5或P<0.01)。甘草酸二铵高、低剂量组大鼠肝组织纤维化病变显著减轻、MMP-2表达显著增强,与模型组比较差异显著(P<0.5或P<0.01)。结论:甘草酸二铵对二甲基亚硝胺诱导的肝纤维化形成具有显著的抑制作用,其机制与抗脂质过氧化损伤、保护肝细胞、增强肝组织MMP-2活性和促进细胞外基质降解有关。
Objective: To observe the effect of diammonium glycyrrhizinate on experimental hepatic fibrosis in rats and its mechanism of action. Methods: The rat model of hepatic fibrosis induced by dimethylnitrosamine was treated with high dose (60 mg / kg) and low dose (15 mg / kg) of glycyrrhizic acid diammonium chloride, (Hyp), malondialdehyde (MDA), serum hyaluronic acid (HA) and laminin (LN) content in liver tissue of rats were observed and compared. The changes of hepatic function, Matrix metalloproteinase 2 (MMP-2) expression. Results: Serum levels of alanine aminotransferase (ALT), aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bilirubin (TBIL) The levels were significantly lower than the model group (P <0.01). The contents of Hyp, MDA, serum HA and LN in liver tissue of high-dose diammonium glycyrrhizinate group were significantly lower than those in model group (P <0.01), but significantly different from those in colchicine group (P <0.5 or P <0.01). Compared with model group, the expression of MMP-2 was significantly reduced (P <0.5 or P <0.01). CONCLUSION: Diammonium glycyrrhizinate can significantly inhibit the formation of hepatic fibrosis induced by dimethylnitrosamine. Its mechanism is related to the anti-lipid peroxidation injury, protecting liver cells, enhancing the activity of MMP-2 in liver and promoting extracellular Matrix degradation related.