The inhibitory effect of compound Q-l on proliferation of MH7A induced by TNF-α and its significance / 中国药理学通报

Aim To investigate the effect of compound Q-L on MH7A based on NF-KB and MAPK signaling pathways and its mechanism. Methods Human rheumatoid arthritis fibroblast synovial cell line (MH7A) was selected as the experimental object. The effect of compound Q-l on the proliferation of MH7A cells was determined by CCK-8 method. The effect of compound Q-l on the migration ability of MH7A cells was detected by Transwell assay. TNF-α solution was used as inducer, and the content of TNF-α and IL-6 in cell supernatant was determined by ELISA. The protein expressions of p65, p-p65, IκBα, P-IκBα, p38, p-p38, ERK, p-ERK, JNK and p-JNK in the cells were determined by Western blot. Results Compound Q-l at different concentrations significantly inhibited the activity of MH7A cells. Compound Q-l significantly inhibited the migration of MH7A cells. Compound Q-l significantly reduced the contents of TNF-α and IL-6 in cell supernatant. Compound Q-l could significantly down-regulate the protein expression levels of p65, p-p65, P-IκBα, p38, p-p38 induced by TNF-α, but had no marked effects on IKBCX, ERK, p-ERK, JNK and p-JNK proteins. Conclusion Compound Q-l can significantly inhibit the proliferation of MH7A cells, reduce the expression of inflammatory cytokines TNF-α and IL-6 in cell supernatant, and down-regulate the protein expressions of p65, p-p65, IKBCX, p-LKBA, p38, p-p38 induced by TNF-α. The possible mechanism of action is related to NF-κB and p38MAPK sig-naling pathways.

Effects of total glucosides of paeony on co-cultured osteoclasts and its mechanisms / 中国药理学通报

s:Aim To study the effects of total gluco-sides of paeony ( TGP) on the differentiation of co-cul-tured osteoclasts and the mechanisms of how TGP influ-ences the osteoclasts. Methods The synovial fibro-blasts and monocytes of peripheral blood in adjuvant-induced arthritic rats were separated and co-cultured to induce osteoclasts. The cells were treated with different TGP dosages (5, 50, 500, 5 000 mg·L-1 , and 50 g ·L-1 ) for 48 h. The proliferation, the TRAP activi-ty, and the bone resorption of osteoclasts were ob-served. The levels of IL-1,TNF-α,M-CSF and RANKL in the supernatants of osteoclasts were detected using ELISA. Meanwhile, the expression of ERK, JNK and p38 was detected by real time PCR. Results The ex-periments revealed that 50, 500, 5 000 mg·L-1 TGP inhibited the osteoclast growth, the TRAP activity, and the resorption pit area in a dose-dependent manner. TGP also inhibited the levels of IL-1 , TNF-α, M-CSF and RANKL in the supernatants and the expression of ERK, JNK and p38 in osteoclasts. The appropriate concentrations were 50 mg·L-1 to 5 000 mg·L-1 and had dose-dependent effects within this range. Conclu-sions TGP regulates the differentiation and activity of co-cultured osteoclasts. The effects of TGP are related to its inhibiting the cytokines secretion of synovial fi-broblasts and the activity of MAPK pathways.