Zhou Lijuan, Zhao Jingyi, Ma Kaile, Hao Rui, Yao Chensi, Gou Xiaowen, Tian Chuanxi, Wan Li, Li Min, Tong Xiaolin
Institute of Metabolic Diseases, Guang'anmen Hospital, China Academy of Chinese Medical Sciences, Beijing, China.
Clinical Medical College, Beijing University of Chinese Medicine, Beijing, China.
Front Immunol. 2025 Jan 7;15:1445924. doi: 10.3389/fimmu.2024.1445924. eCollection 2024.
Non-alcoholic fatty liver disease (NAFLD) constitutes the most prevalent chronic liver disease worldwide. Progression to non-alcoholic steatohepatitis (NASH), the immune cell reservoir within the liver undergoes remodeling, exacerbating liver inflammation and potentially leading to liver fibrosis. Jiangtang Qingre Formula (JQF) is an effective prescription for the clinical treatment of NAFLD. However, its underlying mechanism of action remains unclear.
Using a high-fat diet-induced NAFLD mouse model, we evaluated JQF's effects with biochemical tests and histopathology. Single-cell RNA sequencing and spatial transcriptomics furthered our understanding of NAFLD pathophysiology and JQF's treatment mechanisms.
Our findings initially revealed significant improvements in JQF on hepatic steatosis, inflammation, fibrosis and glucose tolerance in NAFLD mice. Furthermore, significant changes were observed in the immune cells including monocytes, macrophages, and T cells in the livers of NAFLD mice. Notably, regions infiltrated by T cells presented the most severe liver inflammation and fibrosis. Importantly, JQF effectively modulated these immune cells. Advanced subcluster and cell communication analyses identified key macrophage (KCs, MoMFs) and T cell (Tc, Th2) subpopulations in JQF's therapeutic actions. Further SCENIC analysis additionally uncovered the essential transcription factors that regulate these cell subclusters, such as Stat2, Mta3, Eomes, and Etv5.
Overall, our research suggests a promising potential therapeutic agent and identifies critical cell populations and transcription factors that contribute to its therapeutic effects, thereby revealing potential therapeutic targets for NAFLD.
非酒精性脂肪性肝病(NAFLD)是全球最普遍的慢性肝病。进展为非酒精性脂肪性肝炎(NASH)时,肝脏内的免疫细胞库会发生重塑,加剧肝脏炎症并可能导致肝纤维化。降糖清热方(JQF)是临床治疗NAFLD的有效方剂。然而,其潜在作用机制尚不清楚。
我们使用高脂饮食诱导的NAFLD小鼠模型,通过生化检测和组织病理学评估JQF的作用。单细胞RNA测序和空间转录组学进一步加深了我们对NAFLD病理生理学和JQF治疗机制的理解。
我们的研究结果初步显示,JQF对NAFLD小鼠的肝脂肪变性、炎症、纤维化和葡萄糖耐量有显著改善。此外,在NAFLD小鼠肝脏中的免疫细胞(包括单核细胞、巨噬细胞和T细胞)中观察到显著变化。值得注意的是,T细胞浸润的区域呈现出最严重的肝脏炎症和纤维化。重要的是,JQF有效地调节了这些免疫细胞。先进的亚群和细胞通讯分析确定了JQF治疗作用中的关键巨噬细胞(枯否细胞、单核细胞来源的巨噬细胞)和T细胞(细胞毒性T细胞、辅助性T细胞2)亚群。进一步的SCENIC分析还发现了调节这些细胞亚群的关键转录因子,如信号转导和转录激活因子2、转移相关蛋白3、胚外中胚层蛋白和ETS变异体5。
总体而言,我们的研究表明JQF是一种有前景的潜在治疗药物,并确定了对其治疗效果有贡献的关键细胞群体和转录因子,从而揭示了NAFLD的潜在治疗靶点。