Cigu Xiaozhi Prescription Alleviates NASH Liver Fibrosis by Inhibiting the Activation of the Hedgehog Signaling Pathway
10.14148/j.issn.1672-0482.2025.0936
- VernacularTitle:慈菇消脂方通过抑制Hedgehog信号通路激活缓解非酒精性脂肪性肝炎肝纤维化
- Author:
Zhen REN
1
;
Yongjia YANG
;
Cai GUO
;
Yujie ZHANG
;
Yanhua MA
Author Information
1. 甘肃中医药大学医学信息工程学院,甘肃 兰州 730000
- Publication Type:Journal Article
- Keywords:
non-alcoholic steatohepatitis;
liver fibrosis;
Hedgehog signaling pathway;
Cigu Xiaozhi Prescription;
hepatic stellate cells
- From:
Journal of Nanjing University of Traditional Chinese Medicine
2025;41(7):936-945
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVE To explore the potential mechanism of Cigu Xiaozhi Prescription(CGXP)in the treatment of non-alco-holic steatohepatitis(NASH)liver fibrosis.METHODS A NASH mouse model was established.The degree of liver enlargement was evaluated by calculating the liver index.Hematoxylin-eosin(HE)and Masson staining were used to observe the degree of liver fibro-sis.In addition,immunohistochemistry was employed to detect the expression of liver fibrosis-related proteins,including α-SMA,Collagen 1,MMP2,and MMP9.Western blot and qPCR techniques were used to detect the expression levels of HIF-1α,E-cadher-in,N-cadherin,Shh,Smo,Gli1,and Gli2 in the mouse liver.The alkaline hydrolysis method was used to measure the content of liv-er hydroxyproline.RESULTS CGXP could effectively reduce the liver index(P<0.001),alleviate liver enlargement and inflamma-tion,and significantly improve the pathological damage of liver tissue in mice with liver fibrosis.CGXP significantly decreased the ex-pression levels of liver fibrosis-related proteins α-SMA,Collagen 1,MMP2 and MMP9(P<0.01,P<0.000 1);reduced the levels of HIF-1α,E-cadherin,N-cadherin,Shh,Smo,Gli1,and Gli2,and the therapeutic effect of high-dose CGXP was particularly significant(P<0.05,P<0.01,P<0.001,P<0.000 1).CONCLUSION CGXP can relieve NASH liver fibrosis in mice by reducing the liver index,alleviating inflammation,and improving tissue pathological damage.The mechanism may be related to the inhibition of the Hedgehog signaling pathway,which alters the activation and proliferation of hepatic stellate cells and reduces the synthesis and dep-osition of extracellular matrix.
