Effect of Tongbi Granules on Inflammatory Reaction and Expression of NLRP3 Inflammatory Bodies in TypeⅡ Collagen Arthritis Mice

OBJECTIVE To explore the mechanisms of Tongbi Granules on rheumatoid arthritis (RA) in the type Ⅱ collagen-induced arthritis (CIA) mice model. METHODS 60 male mice were randomly divided into 6 groups (n=10)， including normal group， blank control group， high dose group， medium dose group， low dose group and tripterygium polyglycoside group. The CIA model was established by two injections of 0.1 mL CⅡ emulsion. Then， the mice were administered with high， medium and low doses of Tongbi Granules of 50 g/kg， 25 g/kg and 12.5 g/kg， respectively， after the model was established successfully. While， the model group and the normal group were given the same volume of saline， tripterygium glycoside group were given 0.12 g/kg tripterygium glycoside suspension， which once a day and sustained 22 days. The degree of foot swelling in CIA mice was observed by helical micromanometer. The proliferation and adhesion of spleen cells and T lymphocytes were detected by MTT assay. The effects of radiotherapy on the proliferation of synovial cells containing IL-1β，TNF-α levels were detected. Western blot was used to detect the expression of NLRP3 inflammatory bodies in synovial tissues. RESULTS Compared with the normal group， the swelling of the joint appeared on the 13th day after the second immunization. Compared with the blank control group， the high dose group and the tripterygium polyglycoside group could significantly reduce the degree of foot swelling in the CIA model mice， and could significantly inhibit the spleen cell proliferation and its adhesion ability， while still inhibiting the culture Synovial cell proliferation and reduce the synovial cell culture supernatant contained in the IL-1β，TNF-α content. Also， it inhibited the expression of NLRP3 inflammatory body in synovial tissue. CONCLUSION The high and medium dose groups of Tongbi Granules may inhibit the expression of NLRP3 inflammatory body to reduce the proliferation of synovial cells and regulate the formation of inflammatory factors， thereby inhibiting the inflammatory response of RA and relieving joint injury.