[Effect of Xinfeng Capsule in Improving Blood Stasis State of OA Patients]

Objective To observe the relationship between blood stasis state and activation of nuclear factor-κ-gene binding (NF-κB) signaling pathway/miRNA-146 in osteoarthritis (OA) patients and the effect of Xinfeng Capsule (XFC) on them. Methods Totally 70 OA patients were assigned to the treatment group and the control group according to random number table, 35 in each group. Patients in the treatment group took XFC, 3 pills each time, 3 times per day, while those in the control group took Glucosamine, 1 pill each time, 3 times per day. The therapeutic course for all was 3 months. Serum con- tents of p50, p65, inhibitor of nuclear factor κB O (IκBα) , nuclear factor kappa B activator 1 (Act1) , TGF-β-activated kinase 1 (TAK1) , IL-1, IL-17, IL-10, and thromboxane A₂(TXA₂) , prostacycline (PGI₂) were detected by ELISA. mRNA levels of Act1 , p65, p50, and TAK1 were detected using fluorescent quantitative PCR. The protein levels of p50 and p65 were detected using Western blot. The level of miRNA- 146 was detected using in one-step PCR. Results (1) Compared with pre-treatment in the same group, the levels of blood stasis score, platelets (PLT) , D-dimer (D-D) , TXA₂, IL-1, IL-17, high-sensitivity C- reactive protein (hs-CRP), and erythrocyte sedimentation rate (ESR) all decreased; mRNA levels of p50, p65, Act1, and TAK1 were lowered; protein expressions of p50 and p65 decreased; serum levels of miRNA-146 decreased; activated partial thromboplastin time (APTT) , prothrombin time ( PT) , prosta- glandin 2 (PGI₂), IL-10 increased in the two groups after treatment with statistical difference (P <0. 05, P <0. 01). Compared with the control group, the levels of blood stasis score, PLT, FIB,TXA₂, IL-17, hs- CRP, and ESR were lowered; mRNA expressions of p65 and TAK1 were lowered; protein expressions of p50 decreased; levels of PT and PGI₂ increased in the treatment group after treatment (P <0. 05, P < 0.01). Conclusion XFC could regulate the immunity and restore the equilibrium of cytokine network, and protect vascular endothelial cells possibly by up-regulating miRNA-146 expression and inhibiting acti- vation of NF-κB signaling pathway, thus improving blood stasis state of OA.