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许多慢性肝脏疾病都会发生肝纤维化,但是目前尚缺乏对肝纤维化切实有效的治疗手段。实验发现,Flk1(fetalliverkinase)阳性间充质干细胞(MSC)能够减轻四氯化碳(CCl4 )所致小鼠肝纤维化。取雄性BALB c小鼠骨髓,分离培养Flk1+ MSC ,用CCl4 制作雌性小鼠肝纤维化模型,在CCl4 损伤后立即或1周后经尾静脉注射Flk1+ MSC ,2或5周后检测受体小鼠肝脏的纤维化程度和供体细胞的植入。结果发现,CCl4 损伤后立即注射Flk1+ MSC ,可以使肝脏损伤程度明显减轻,减少胶原沉积,使肝脏羟脯氨酸含量及血清纤维化指标显著下降;而损伤1周后注射细胞则无明显变化。免疫荧光、PCR和荧光原位杂交方法证实,在受体肝脏中有供体细胞植入,呈上皮细胞形态,并表达白蛋白,但是数量很少。因此,Flk1+ MSC具有潜在的植入肝组织的能力,并可能启动肝组织的内源性修复,减轻CCl4 导致的肝纤维化。
Liver fibrosis occurs in many chronic liver diseases, but there is currently no effective treatment for liver fibrosis. It was found that Flk1 (fetalliverkinase) -positive mesenchymal stem cells (MSCs) can reduce hepatic fibrosis induced by carbon tetrachloride (CCl4) in mice. Bone marrow of male BALB c mice was isolated and cultured. Flk1 + MSCs were isolated and cultured. CCl4 female mice were used to make hepatic fibrosis model. Flk1 + MSCs were injected into tail vein immediately or 1 week after CCl4 injury. Liver fibrosis and donor cell engraftment. The results showed that injection of Flk1 + MSCs immediately after CCl4 injury significantly reduced the degree of hepatic injury, reduced collagen deposition, and markedly decreased the content of hydroxyproline and the serum fibrosis index. However, there was no significant change in the injected cells after 1 week of injury. Immunofluorescence, PCR and fluorescence in situ hybridization confirmed donor cell engraftment, epithelial morphology and albumin expression in the recipient liver but in small numbers. Thus, Flkl + MSC has the potential of implanted liver tissue and may initiate endogenous repair of liver tissue, reducing CCl4-induced hepatic fibrosis.