Hepatoprotective effects of Yinchenzhufu decoction on intrahepatic cholestasis liver injury in mice induced by ANIT via suppressing TLR4/NF-κB pathway
10.12092/j.issn.1009-2501.2020.06.001
- VernacularTitle: 茵陈术附汤抑制TLR4/NF-κB通路对α-萘异硫氰酸酯诱导肝内胆汁淤积症模型小鼠肝损伤的保护作用
- Author:
Qian WANG
1
Author Information
1. Shuguang Hospital Affiliated to Shanghai University of Traditional Chinese Medicine
- Publication Type:Journal Article
- Keywords:
Cholestasis liver injury;
TLR4/NF-κB pathway;
Yinchenzhufu decoction
- From:
Chinese Journal of Clinical Pharmacology and Therapeutics
2020;25(6):601-609
- CountryChina
- Language:Chinese
-
Abstract:
AIM: To investigate the hepatoprotective effects of Yinchenzhufu decoction (YCZFD) via TLR4/NF-κB pathway on the hepatic injury in alpha-naphthyisothiocyanate (ANIT)-induced intrahepatic cholestasis mice. METHODS: Male C57BL/6 mice were administered with YCZFD for consecutive 10 days, and intrahepatic cholestasis mice model was induced by orally given ANIT at dose of 75 g/kg on the seventh day. On the last day, the blood samples and liver samples were collected 2 hours after oral administration of YCZFD. The serum biochemical index, liver histopathology, the change of bile acid contents in mice liver, and the expression of relative proteins in TLR4/NF-κB pathway were determined. RESULTS: Compared with the model group, YCZFD treatment group significantly improved the hepatic necrosis and reduced the inflammatory cell infiltration. The plasma alanine aminotransferase (ALT) and aspartate aminotransferase (AST), alkaline phosphatase (ALP), total bile acid (TBA), and total bilirubin (TBIL) levels were significantly decreased, and the free and conjugated bile acids were both reduced. The expression of TLR4, IL-1β, IL-6, TNF-α, and MCP-1 were significantly decreased. CONCLUSION: YCZFD presents hepatoprotective effects on the hepatic injury in ANIT-induced intrahepatic cholestasis mice, which may be related to inhibiting the TLR4/NF-κB pathway, reducing the intrahepatic bile acids, and suppressing the inflammatory reaction.
