Bai Chongyang, Song Xiaojing, Yan Jiexi, Xu Jun, Zhou Yongqiang, Sun Zongbin, Zheng Qiuxia, Zhang Yue, Chen Ruixi, Jin Xiaoyi, Shao Yi, Xie Yande, Yang Lele, Zhong Fupeng, Zhang Yuting, Li Jiatai, Li Runfeng, Yan Shaolin, Li Xun
The First School of Clinical Medicine, Lanzhou University, Lanzhou 730000, China.
Department of General Surgery, The First Hospital of Lanzhou University, Lanzhou 730000, China.
Biomedicines. 2025 Apr 9;13(4):910. doi: 10.3390/biomedicines13040910.
: Liver regeneration is a critical measure of liver health and plays an essential role in inhibiting the progression of fibrotic lesions and preventing liver failure after hepatocellular carcinoma surgery. However, there are no approved drugs to address this clinical challenge. : The effects of TUDCA on liver regeneration and fibrosis were studied using BRL-3A cells, a partial hepatectomy (PH) rat liver regeneration model, and a carbon tetrachloride (CCl)-induced liver fibrosis model. GATA3-knockdown BRL-3A cells were employed to assess the role of GATA3 in TUDCA-induced proliferation. : TUDCA promoted the proliferation of BRL-3A cells and enhanced liver regeneration in PH rats while ameliorating liver fibrosis in CCl-treated rats. Additionally, the knockdown of GATA3 eliminated the proliferative effect of TUDCA on BRL-3A cells. : TUDCA promotes liver regeneration and alleviates liver fibrosis by activating GATA3.
肝脏再生是肝脏健康的关键指标,在抑制纤维化病变进展以及预防肝细胞癌手术后肝衰竭方面发挥着重要作用。然而,目前尚无获批用于应对这一临床挑战的药物。
使用BRL-3A细胞、部分肝切除术(PH)大鼠肝脏再生模型以及四氯化碳(CCl)诱导的肝纤维化模型研究了牛磺熊去氧胆酸(TUDCA)对肝脏再生和纤维化的影响。采用GATA3基因敲低的BRL-3A细胞来评估GATA3在TUDCA诱导的增殖中的作用。
TUDCA促进了BRL-3A细胞的增殖,增强了PH大鼠的肝脏再生,同时改善了CCl处理大鼠的肝纤维化。此外,GATA3基因敲低消除了TUDCA对BRL-3A细胞的增殖作用。
TUDCA通过激活GATA3促进肝脏再生并减轻肝纤维化。