Analgesic and anti-inflammatory effects of Hanshibi tablet in mice and its effect on synovial pathology in a rat model of rheumatoid arthritis.
- Author:
Chun JI
1
;
Zeng-hui XIN
;
Qi-fu WU
;
Li TONG
Author Information
- Publication Type:Journal Article
- MeSH: Animals; Anti-Inflammatory Agents, Non-Steroidal; pharmacology; therapeutic use; Arthritis, Rheumatoid; drug therapy; pathology; Drugs, Chinese Herbal; pharmacology; therapeutic use; Female; Male; Mice; Phytotherapy; Random Allocation; Rats; Rats, Sprague-Dawley; Synovial Membrane; pathology; Tablets
- From: Journal of Southern Medical University 2009;29(12):2497-2503
- CountryChina
- Language:Chinese
-
Abstract:
OBJECTIVETo evaluate the analgesic and anti-inflammatory effects of Hanshibi tablet in Kunming mice and the effect of the tablet in ameliorating synovial pathology in a rat model of rheumatoid arthritis (RA).
METHODSStretching test, capillary permeability and ear swelling test of Kunming were performed to observe the analgesic and anti-inflammatory effects of Hanshibi tablet administered intragastrically at different doses. In a SD rat model of RA induced by heat-inactivated Mycobacterium tuberculolytic H37Ra (Mtb), the effect of the tablet on the symptoms and progression of arthritis was observed regularly, and the numbers of the peripheral white blood cells, platelets and lymphocytes and mononuclear cells were measured. HE staining was used to examine the pathology of the rat ankle, and flow cytometry performed to monitor the changes in the T lymphocyte subsets.
RESULTSHanshibi tablet treatment reduced the writhing response frequency and prolonged the stretching latency of Kunming mice. The tablet also inhibited the acetic acid-induced increase in capillary permeability and ear swelling. In the rat model of RA, administration of the tablet resulted in reduced ratio of CD4(+)/CD8(+), and significantly ameliorated synovial pathology.
CONCLUSIONHanshibi tablet has obvious analgesic and anti-inflammatory effects and ameliorates the synovial pathology in the rat model of RA possibly by regulating CD4(+)/CD8(+) balance.