The Pathological Effect Of PengCao Removing Bi-syndrome Decoction On Synovial Inflamation And Bone Erosion Of Rats With Collagen-Induced Arthritis

Objective:To study the mechanism of PengCao Removing Bi-syndrome Decoction on Rheumatoid Arthritis(RA) from the pathological and immunohistochemical perspective by observing Histopathology affect on synovial tissue and the regulation mechanism of bone erosion of rats with collagen-induced arthritis(CIA) treated by the decoction.Methods:Clean level Wistar rats,60, male and female evenly, weigtht(110±20)g, Random out 10 rats as blank group, the remaining 50 rats for replication collagen inductive arthritis (CIA) model,7 days after causing inflammation began to observe and record systemic articular damage degree, every 7 days record 1 times, the rats with arthritis index (AI)> 5 points are made mould success.Then we divide them into Chinese high, medium, low group, tripterygium glycosides(TG) group and model group, observe 6 weeks, evaluate the arthritis index(AI), the pathological changes of synovial tissue and the Osteoprotegerin(OPG),Receptor Activator of NF-κB Ligand (RANKL) expressions in cartilage of rats.ResuIt: Compared with model group, the AI of Chinese group and Tripterygium group was significantly lower (P<0.05, P<0.01), pathological changes in synovial tissue scores were significantly different, (P<0.05, P<0.01), through pathological morphology observation, PengCao Removing Bi-syndrome Decoction of high, medium and dose group and TG group, synovial cell hyperplasia degree is lower than model group significantly, inflammatory cells infiltration and synovial vasculitis performance were significantly reduced.Conclusion:PengCao Removing Bi-syndrome Decoction could reduce the AI of rats, and inhibit synovial cell proliferation, fibrous tissue hyperplasia, inflammatory cell infiltration and macrophage infiltration, which is a pure compound preparations worth of a further development and research.The RA regulatory mechanisms of Articular bone erosion may be related to inhibition of RANKL expression in articular cartilage of rat with CIA and of no obvious effect on the expression of OPG.