Studies have shown that human umbilical cord mesenchymal stem cells (hUCMSCs) could ameliorate liver fibrosis (LF) through inhibiting the activation of hepatic stellate cells (HSCs). However, the specific mechanisms have not been studied clearly. The purpose of this study was to explore the possible mechanism of hepatocyte growth factor (HGF)-transfected hUCMSCs in inhibiting the proliferation and activation of HSCs-T6. The upper and lower double-cell coculture system was established among HGF-hUCMSCs, LV5-NC-hUCMSCs, hUCMSCs, and HSCs-T6 in experimental groups; HSCs-T6 were cultured alone as control group. After coculturing for 1, 2, and 3 days, results showed that HGF-transfected hUCMSCs could decrease cell viability of HSCs-T6 and promote apoptosis; inhibit their activation and reduce the expression of Collagen I, Collagen III, TGF-β1, Smad2 and Smad3, which may be related to inhibiting the activation of TGF-β1/Smads signaling pathway. These findings suggested that HGF-transfected hUCMSCs may be used as an alternative and novel therapeutic approach for the treatment of LF.

中文翻译：

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肝细胞生长因子转染人脐带间充质干细胞通过调控转化生长因子-β1/Smads信号通路对肝星状细胞的影响

研究表明，人脐带间充质干细胞（hUCMSCs）可通过抑制肝星状细胞（HSCs）的活化来改善肝纤维化（LF）。但是，具体的机制还没有被研究清楚。本研究旨在探讨转染肝细胞生长因子(HGF)的hUCMSCs抑制HSCs-T6增殖和活化的可能机制。实验组HGF-hUCMSCs、LV5-NC-hUCMSCs、hUCMSCs、HSCs-T6之间建立上下双细胞共培养体系；单独培养HSCs-T6作为对照组。共培养1、2、3天后，结果表明转染HGF的hUCMSCs可以降低HSCs-T6的细胞活力，促进细胞凋亡；抑制它们的活化并降低胶原蛋白 I、胶原蛋白 III、TGF-β1 的表达，Smad2和Smad3，可能与抑制TGF-β1/Smads信号通路的激活有关。这些发现表明，HGF 转染的 hUCMSCs 可用作治疗 LF 的替代和新型治疗方法。