目的探讨18α甘草酸(18αGL)对CCl4诱导的肝纤维化大鼠的I型胶原的调控作用。方法采用40%CCl4皮下注射方法建立肝纤维化大鼠模型,分为正常组、肝纤维化模型组和18αGL干预组。采用免疫组织化学和实时PCR分析I型胶原表达情况。Signal-Net网络分析发现与I型胶原组分COL1A1和COL1A2直接相关的基因,实时PCR分析18αGL干预后相关基因表达情况。结果 18αGL能够改善纤维化大鼠I型胶原相关COL1A1和COL1A2的mRNA水平,并且能减少I型胶原的分布。Signal-Net网络分析发现与COL1A1和COL1A2直接相关的基因中,与TGF-β/Smad、Rho/rock、MAPK、PDGF和MMP等信号通路相关,动物体内18αGL可引起RAC、RHOA、HSPB、SMAD3、SP-1和MMP2、MMP9转录水平的下调。结论 18αGL能够显著减少纤维化大鼠肝脏I型胶原的表达,并且从多通路抑制I型胶原COL1A1和COL1A2表达,从而可以多层次,多靶点的改善胶原和影响肝纤维化进程。 Objective To investigate the regulatory effect of 18αglycolic acid (18αGL) on type I collagen in CCl4-induced hepatic fibrosis rats. Methods 40% CCl4 subcutaneously injected rat liver fibrosis model was established, divided into normal group, liver fibrosis model group and 18αGL intervention group. Type I collagen expression was analyzed by immunohistochemistry and real-time PCR. Signal-Net network analysis found that the type I collagen components COL1A1 and COL1A2 directly related genes, real-time PCR analysis of 18αGL intervention related gene expression. Results 18αGL can improve the mRNA expression of collagen type Ⅰcollagen-related COL1A1 and COL1A2 in fibrotic rats and reduce the distribution of type I collagen. Signal-Net network analysis found that genes related directly to COL1A1 and COL1A2 are related to the signaling pathways such as TGF-β / Smad, Rho / rock, MAPK, PDGF and MMP. In animals, 18αGL can cause RAC, RHOA, HSPB, SMAD3, SP-1 and MMP2, MMP9 transcriptional level down. Conclusion 18αGL can significantly reduce the expression of type Ⅰ collagen in hepatic fibrosis rats and inhibit the expression of collagen type Ⅰcollagen COL1A1 and COL1A2 from multiple pathways, which can improve collagen and affect hepatic fibrosis process in multiple levels and targets.