Cell-type-specific role of STAT3 in non-alcoholic steathepatitis

通过使用肝细胞特异性STAT 3敲除小鼠和巨噬细胞/中性粒细胞特异性STAT 3敲除小鼠来检查STAT 3的细胞类型特异性作用。基因敲除小鼠和对照野生型小鼠均喂食蛋氨酸-胆碱缺乏饮食，这是鼠NASH模型。我们已经证明，肝细胞中STAT 3的激活通过抑制SREBP 1c的激活来预防脂肪变性。另一方面，我们已经揭示了巨噬细胞/中性粒细胞中STAT 3的激活加速了肝脏中的炎症，同时它通过肝细胞中的STAT 3激活来防止脂肪变性。

The cell type specific role of STAT3 was examined by using hepatocyte-specific STAT3 knockout mice and macrophage/neutrophil specific STAT3 knockout mice. Both knockout mice and control wild type mice were fed with methionine-choline deficient diet, which is a murine NASH model. We have shown activation of STAT3 in hepatocyte prevents steatosis by inhibiting SREBP1c activation. On the other hand, we have revealed activation of STAT3 in macrophage/neutrophil accelerates inflammation in the liver, while it prevents steatosis by STAT3 activation in hepatocytes.