Study of Dicliptera Chinensis Polysaccharide in Counteracting Liver Injury Induced by Antituberculosis Drugs
10.13359/j.cnki.gzxbtcm.2014.06.023
- VernacularTitle:狗肝菜多糖对抗结核药物致肝损伤的研究
- Author:
Ya GAO
;
Mingli ZHONG
;
Jialiang ZHONG
;
Kefeng ZHANG
- Publication Type:Journal Article
- Keywords:
Dicliptera chinensis polysaccharide/pharmacology;
Liver injury/TCD therapy;
Liver/pathology;
Disease models,animal;
Mice
- From:
Journal of Guangzhou University of Traditional Chinese Medicine
2014;(6):953-956
- CountryChina
- Language:Chinese
-
Abstract:
Objective To study the therapeutic effect and mechanism of Dicliptera chinensis polysaccharide ( DCP) on liver injury induced by antituberculosis drugs. Methods Sixty mice were randomly divided into six groups, namely normal control group, model group, glucurolactone group (in the dosage of 200 mg·kg-1·d-1), and high-, middle- and low-dose DCP groups ( in the dosage of 600, 400, 200 mg·kg-1·d-1, respectively). Except for the normal control group, the rats in the other groups were given intragastric administration of isoniazid and rifampicin ( 100 mg/kg) to induce liver injury model, and were simultaneously treated with corresponding agents, once a day. On the experiment day 30, the blood and liver tissue were sampled. The serum levels of alanine aminotransferase ( ALT) , aspartate aminotransferase ( AST) , alkaline phosphatase ( AKP) and microsomal nitric oxide ( NO) were detected by biochemical method. The contents of tumor necrosis factor alpha (TNF-α) and interleukin 6 (IL-6) in liver tissue were determined by enzyme-linked immunosorbent assay ( ELISA) , and the hepatic histopathology was observed after HE staining. Results In DCP groups, the hepatic pathological changes of the mice were improved, the number of the inflammatory cells was reduced, and the activities of serum ALT, AST and AKP as well as the contents of hepatic TNF-α, IL-6 and NO were reduced ( P<0.05 or P<0.01 compared with those in the model group). Conclusion Dicliptera chinensis polysaccharide is effective for liver injury induced by antituberculosis drug, and the mechanism may be associated with its anti-inflammatory action.
