Molecular basis pathogenesis of blood stasis in rheumatoid arthritis based on thromboxane synthase

LI Wen-jie; HUANG Run-yue; CHU Yong-liang; HE Xiao-hong; HUANG Qing-chun

Abstract：Objective To investigate the molecular basis of pathogenesis of blood stasis in rheumatoid arthritis (RA).Methods Tumor necrosis factor alpha (TNF-α) was used to induce fibroblast -like synoviocytes MH7A of RA, so as to establish an in vitro model of RA.By means of MTS method, the effect of methotrexate (MTX) and sinome-nine ( SIN) on proliferation of MH7A cells was detected .The effect of different concentrations of MTX and SIN on expres-sion of alpha actinin-1 (ACTN1), thromboxane synthase (TxAS), cyclooxygenase -2 (COX-2) was detected using Western blot .The expression of ACTN 1 and TxAS in synovial tissues of different syndrome types of RA was also detected . Results MTS showed that both MTX and SIN, at 50, 200, 400 μg/mL, could inhibit the proliferation of MH7A, under treatment of 24, 48 and 72 h.The results of Western blot showed that expression of ACTN 1, TxAS and COX-2 was in-hibited by MTX and SIN , which was more remarkable in TNF -α-induced model .And the trends of expression of ACTN1, TxAS and COX-2 were consistent in the MH7A cell line.Expressions of ACTN1 and TxAS in synovial tissues of types Hanshizubi and Ganshenbuzu were significantly higher than those of type Shirezubi .Conclusion TxAS can be regu-lated by classical anti-rheumatic agents MTX and SIN , and its expression is consistent with that of ACTN 1, the marker of synovial cell proliferation and invasion in RA .These indicate that TxAS may be part of the molecular basis to the patho-genesis of blood stasis in RA .