Protection of Herba Scutellariae Barbatae against hepatotoxicity induced by Rhizoma Dioscoreae Bulbiferae and its mechanism
10.16438/j.0513-4870.2015-0500
- VernacularTitle:半枝莲对黄药子肝毒性的保护作用及其机制
- Author:
Cheng-wei NIU
1
;
Li-li JI
1
;
Zheng-tao WANG
1
Author Information
1. The Shanghai Key Laboratory for Complex Prescription, The Ministry of Education Key Laboratory for Standardization of Chinese Medicines, and The State Administration of Traditional Chinese Medicine Key Laboratory for New Resources and Quality Evaluation of Chinese Medicines, Institute of Chinese Materia Medica, Shanghai University of Traditional Chinese Medicine, Shanghai 201203, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
Rhizoma Dioscoreae Bulbiferae;
Herba Scutellariae Barbatae;
hepatotoxicity;
inflammatory injury
- From:
Acta Pharmaceutica Sinica
2016;51(3):373-
- CountryChina
- Language:Chinese
-
Abstract:
This study was conducted to test the protective activity of ethanol extract of Herba Scutellariae Barbatae (SE) against hepatotoxicity induced by Rhizoma Dioscoreae Bulbiferae in mice and its mechanism. SE was orally given to mice at various doses, and ethyl acetate fraction of Rhizoma Dioscoreae Bulbiferae (EF, 450 mg·kg-1) was also orally given at the same time. After 11 days, serum levels of alanine/aspartate aminotransferase (ALT/AST), alkaline phosphatase (ALP), total protein (TP) and albumin (ALB) were measured, and liver histological examination was conducted. Liver glutathione (GSH) amount, myeloperoxidase (MPO) activity and serum tumor necrosis factor-α (TNF-α), interleukin-6 (IL-6) and interferon-γ (IFN-γ) levels were measured. The expression of heme oxygenase-1 (HO-1), inhibitor of kappa B (IκB) and nuclear factor κB (NF-κB) p65 were determined by Western blot. The results showed that SE (200 mg·kg-1) reversed EF-induced changes of serum ALT, AST, ALP, TP and ALB. Liver histology also suggests the protection of SE against EF-induced liver injury. SE reduced the increased MPO activity in liver and TNF-α, IL-6, IFN-γ contents in serum, and blocked the decrease in IκB expression and subsequent increase in phosphorylation and nuclear translocation of p65 induced by EF. EF increased liver GSH amount and heme oxygenase-1 (HO-1) protein expression in mice. SE increased liver GSH amount, but decreased the expression of HO-1. All those results suggest that SE alleviates liver injury induced by consecutive administration of EF by alleviating inflammatory injury via inhibiting NF-κB signaling pathway and elevating antioxidant capacity.
