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目的:探讨移植骨髓基质细胞(BMSCs)减轻小鼠肝纤维化的作用.方法:♂BALB/c小鼠BMSCs分离培养及经门静脉移植到♀BALB/c小鼠肝脏,二乙基亚硝胺诱导肝纤维化.60只♀小鼠随机分为对照组,模型组及治疗组.3mo后测定ALT、AST、透明质酸酶(HA)和层黏连蛋白(LN)浓度,及肝脏羟基脯氨酸(Hyp)含量.免疫组化检测肝脏α-平滑肌肌动蛋白(α-SMA)表达,及荧光原位杂交鉴定移植的BMSCs向肝细胞的分化.结果:BMSCs在添加肝细胞生长因子(HGF)的培养基中体外培养能分化为肝细胞样细胞.与模型组相比,移植BMSCs能显著降低血清ALT、AST、HA和LN的水平以及肝脏Hyp含量和α-SMA的表达(208±44U/L vs 341±66U/L,372±84U/L vs 506±81U/L,289±74μg/L vs 362±83μg/L,178±48μg/L vs 232±63μg/L,900±141mg/g liver vs 1255±205 mg/g liver,均P<0.01).荧光原位杂交显示DEN诱导的损伤肝脏中有骨髓来源的肝细胞,3 mo后10%的肝细胞来源于BMSCs.结论:在肝纤维化模型中,经门静脉移植的BMSCs能分化为肝细胞,有效地恢复肝功能和减轻肝纤维化.
OBJECTIVE: To investigate the effect of transplanted bone marrow stromal cells (BMSCs) on the reduction of hepatic fibrosis in mice.Methods: BMSCs of BALB / c mice were isolated and cultured, and transplanted into the livers of BALB / c mice via portal vein. Diethylnitrosamine Liver fibrosis.All 60 mice were randomly divided into control group, model group and treatment group.The levels of ALT, AST, HA and LN were measured after 3 months, and liver hydroxyproline (Hyp) were detected by immunohistochemistry, the expression of α-smooth muscle actin (α-SMA) in liver was detected by immunohistochemistry, and the differentiation of transplanted BMSCs into hepatocytes was identified by fluorescence in situ hybridization.Results: BMSCs were cultured in the presence of hepatocyte growth factor ) Could differentiate into hepatocyte-like cells in vitro.Compared with the model group, transplanted BMSCs could significantly reduce the levels of serum ALT, AST, HA and LN as well as hepatic Hyp content and α-SMA expression (208 ± 44U / L vs 341 ± 66 U / L, 372 ± 84 U / L vs 506 ± 81 U / L, 289 ± 74 μg / L vs 362 ± 83 μg / L, 178 ± 48 μg / L vs 232 ± 63 μg / L, 900 ± 141 mg / liver vs 1255 ± 205 mg / g liver, all P <0.01) .Fluorescence in situ hybridization showed that there were bone marrow-derived hepatocytes in DEN-induced liver injury, and 10% of hepatocytes originated from BMSCs after 3 months. : In a liver fibrosis model, BMSCs transplanted via the portal vein can differentiate into hepatocytes, effectively recovering liver function and reducing liver fibrosis.