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首页> 外文期刊>Cell biology international. >Hepatogenic differentiation of mesenchymal stem cells in a rat model of thioacetamide-induced liver cirrhosis
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Hepatogenic differentiation of mesenchymal stem cells in a rat model of thioacetamide-induced liver cirrhosis

机译：硫代乙酰胺诱导的肝硬化大鼠模型中间充质干细胞的肝细胞分化

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Implantation of bone-marrow-derived MSCs (mesenchymal stem cells) has emerged as a potential treatment modality for liver failure, but in vivo differentiation of MSCs into functioning hepatocytes and its therapeutic effects have not yet been determined. We investigated MSC differentiation process in a rat model of TAA (thioacetamide)-induced liver cirrhosis. Male Sprague-Dawley rats were administered 0.04% TAA-containing water for 8 weeks, MSCs were injected into the spleen for transsplenic migration into the liver, and liver tissues were examined over 3 weeks. Ingestion of TAA for 8 weeks induced micronodular liver cirrhosis in 93% of rats. Injected MSCs were diffusely engrafted in the liver parenchyma, differentiated into CK19 (cytokeratin 19)- and thy1-positive oval cells and later into albumin-producing hepatocyte-like cells. MSC engraftment rate per slice was measured as 1.0-1.6%. MSC injection resulted in apoptosis of hepatic stellate cells and resultant resolution of fibrosis, but did not cause apoptosis of hepatocytes. Injection of MSCs treated with HGF (hepatocyte growth factor) in vitro for 2 weeks, which became CD90-negative and CK18-positive, resulted in chronological advancement of hepatogenic cellular differentiation by 2 weeks and decrease in anti-fibrotic activity. Early differentiation of MSCs to progenitor oval cells and hepatocytes results in various therapeutic effects, including repair of damaged hepatocytes, intracellular glycogen restoration and resolution of fibrosis. Thus, these results support that the in vivo hepatogenic differentiation of MSCs is related to the beneficial effects of MSCs rather than the differentiated hepatocytes themselves.
机译：骨髓间充质干细胞（间充质干细胞）的植入已成为潜在的肝衰竭治疗方法，但尚未确定将MSCs体内分化为功能性肝细胞及其治疗效果。我们调查了TAA（硫代乙酰胺）诱导的肝硬化大鼠模型中的MSC分化过程。雄性Sprague-Dawley大鼠被给予含0.04％TAA的水8周，将MSCs注入脾脏以经脾转移到肝脏，并在3周内检查肝组织。摄入TAA 8周可导致93％的大鼠发生小结节性肝硬化。注射的MSCs弥漫植入肝实质，分化为CK19（细胞角蛋白19）和thy1阳性卵圆形细胞，然后分化为产生白蛋白的肝细胞样细胞。测得每片的MSC植入率为1.0-1.6％。 MSC注射导致肝星状细胞凋亡并导致纤维化消退，但未引起肝细胞凋亡。体外注射用HGF（肝细胞生长因子）处理2周的MSC，其变为CD90阴性和CK18阳性，导致肝细胞分化的时间顺序延长了2周，并降低了抗纤维化活性。 MSCs向祖卵形细胞和肝细胞的早期分化导致各种治疗效果，包括修复受损的肝细胞，细胞内糖原的恢复和纤维化的解决。因此，这些结果支持了MSC的体内肝发生分化与MSC的有益作用有关，而不是与分化的肝细胞本身有关。

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