BackgroundTraditional Chinese medicine (TCM) formula Bi-Qi capsule (Bi-Qi) is a commonly prescribed drug to treat rheumatoid arthritis (RA). However, the mechanism of Bi-Qi-mediated amelioration of RA pathogenesis is still a mystery. Collagen induced arthritis (CIA) in rats is an established model that shares many similarities with RA in humans. In this study we investigated the effect of Bi-Qi on the pathogenesis of CIA in rats.MethodsCIA was developed in Sprague-Dawley (S.D) rats (n = 60, female) and used as a model resembling RA in humans. Rats were treated with a high or moderate dose of Bi-Qi, or methotrexate (MTX). Effects of the treatment on local joint and systemic inflammation, synovial hyperplasia, cartilage destruction, and other main features in the pathogenesis of CIA were analyzed.ResultsInflamed and swollen ankles and joints were observed in arthritic rats, while Bi-Qi or MTX treatment alleviated these symptoms. Only the Bi-Qi moderate dose decreased RA-induced serum levels of tumor necrosis factor-alpha (TNF-α). Both Bi-Qi and MTX reduced the interleukin (IL)-18 serum level. Protein levels of cartilage oligomeric matrix protein and osteopontin in serum, synovium, and cartilage were elevated in arthritic rats, while Bi-Qi alleviated these effects. Synovial hyperplasia, inflammatory cell infiltration in synovium and a high degree of cartilage degradation was observed in RA, and Bi-Qi or MTX alleviated this effect. Bi-Qi at the moderate dose was the most effective in mitigating CIA-related clinical complications.ConclusionsOur findings showed that Bi-Qi alleviates CIA-induced inflammation, synovial hyperplasia, cartilage destruction, and the other main features in the pathogenesis of CIA. This provides fundamental evidence for the anti-arthritic properties of Bi-Qi and corroborates the use of Bi-Qi TCM formula for the treatment of RA.Electronic supplementary materialThe online version of this article (10.1186/s13075-018-1547-6) contains supplementary material, which is available to authorized users.
BackgroundNew evidence has shown that reduced β2-glycoprotein I (β2GPI) has anti-oxidative stress and anti-inflammatory activity. However, the details are still poorly understood. This study aims to prepare stable reduced β2GPI with its native bioactivity in vitro.MethodsHuman β2GPI was purified from plasma first with perchloric acid precipitation and then purified with a series of chromatography methods including Sephadex G-25 desalting, SP HP, AF-heparin HC-650 M, and Sephacryl S-200. The purified human β2GPI was reduced with thioredoxin-1 (TRX-1) activated by DL-dithiothreitol (DTT). Glutathione (GSH) was selected to block the free thiols in reduced β2GPI. LC/MS was used to verify the location of free thiols. Western blot analysis was used to detect β2GPI immunoreactivity. MTS and flow cytometry were conducted to investigate its biological effect on oxidative-stress-induced death of human umbilical vein endothelial cells (HUVECs). The levels of tumour necrosis factor-alpha (TNF-α),interleukin-6 (IL-6) interleukin-10 (IL-10),interleukin-12P70 (IL-12P70),interferon-gamma (IFN-γ) and monocyte chemoattractant protein −1(MCP-1) in mouse serum were quantified to assess its anti-inflammatory activity in lipopolysaccharide (LPS)-mediated systemic inflammation.ResultsWe obtained approximately 10 mg β2GPI (purity 98.7%) from 200 ml plasma. The protein yield was 0.05 mg/ml plasma. β2GPI was then reduced by TRX-1/DTT in vitro; the free thiols were detected on Cys288 and Cys326 in domain V of β2GPI. The GSH blockage stabilized the reduced β2GPI in vitro. This reduced β2GPI can be recognized by the anti-β2GPI antibody, can significantly reduce the death of HUVECs after H2O2 treatment and can significantly decrease the levels of TNF-α, IL-6,IFN-γ and MCP-1 in mice upon LPS stimulation.ConclusionStable reduced β2GPI can be obtained in vitro by TRX-1 deoxidation followed by the blockage of thiols with GSH. This reduced β2GPI maintains the same immunological activity as oxidized β2GPI and has the ability to counter the oxidative stress induced by H2O2 in HUVECs and inflammation in LPS-mediated inflammation in mice.
Upstream vortex has a significant effect on the secondary flow structure of the downstream turbine in the stage environment. This study investigates the secondary flow structure with non-axisymmetric endwall profiling (NAEW) under the interaction of co-rotating incoming vortex (Vic). A half-delta wing vortex generator is utilized to model Vic. The turbine cascade case which exhibited maximum reduction of the cascade loss with NAEW under no incoming vortex is studied. The mechanism of loss reduction with NAEW under the interaction of Vic is analysed. Vic could decrease the secondary flow near the endwall region by affecting the horseshoe vortex transport in the cascade. However, its loss reduction was lower than the loss increments of Vic itself. The arrival of Vic at the leading edge of the cascade increased the strength of the horseshoe vortex, resulting in a significant increase in loss. Under the interaction of Vic, NAEW decreased the blade loading near endwall region, which resulted in the reduction of cascade loss.
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