Abstract. The present study aimed to construct a rat model of rheumatoid arthritis (RA) to evaluate changes in pathology, the expression of inflammatory factors and regulation of signaling pathways. The protective effect of tetrandrine (Tet) on tissue lesions induced by RA was also investigated. A total of 60 Wistar rats (100-200 g) were randomly divided into six groups (n=10 per group), namely a blank (NC) group, model group, methotrexate (MTX) group (3 mg/kg body weight), high-dose Tet group (31.25 mg/kg body weight), medium-dose Tet group (18.75 mg/kg body weight) and low-dose Tet group (6.25 mg/kg body weight). A rat model of RA was induced via injection of 0.1 ml complete Freund's adjuvant into the right rear toe. Toe swelling rate, arthritis index and immune organ index were calculated. In addition, cyclooxygenase (COX)-2 expression at the mRNA and protein level in the peripheral blood mononuclear cells (PBMCs) of rats were determined by reverse transcription-quantitative polymerase chain reaction and western blot analysis, respectively. Serum concentrations of inflammatory factors were measured using enzyme-linked immunosorbent assays. It was observed that treatment with Tet alleviated the severity of rear toe swelling associated with RA in rats. Furthermore, Tet exerted anti-inflammatory and immunosuppressive effects in the rat model of RA. Tet also reduced the expression of COX-2 in PBMCs and lowered the concentrations of inflammatory factors in the serum of RA rats. The present data indicate that Tet may exert pharmacological effects in the treatment of RA. The mechanism of action of Tet may be associated with the regulation of inflammatory factors and the inhibition of immune organs.

BackgroundQuick diagnosis of smear-negative pulmonary tuberculosis (TB) and extra-pulmonary TB are urgently needed in clinical diagnosis. Our research aims to investigate the usefulness of the interferon-γ release assay (IGRA) for the diagnosis of smear-negative pulmonary and extra-pulmonary TB.MethodsWe performed TB antibody and TB-IGRA tests on 389 pulmonary TB patients (including 120 smear-positive pulmonary TB patients and 269 smear-negative pulmonary TB patients), 113 extra-pulmonary TB patients, 81 patients with other pulmonary diseases and 100 healthy controls. Blood samples for the TB-Ab test and the TB-IGRA were collected, processed, and interpreted according to the manufacturer’s protocol.ResultsThe detection ratio of smear-positive pulmonary TB patients and smear-negative pulmonary TB patients were 90.8% (109 of 120) and 89.6% (241 of 269), respectively. There was no statistically significant difference of its performance between these two sample sets (P > 0.05). The detection ratio of positive TB patients and extra-pulmonary TB patients were 90.0% (350 of 389) and 87.6% (99 of 113), respectively, which was not significantly different (P > 0.05).ConclusionsIn this work, the total detection ratio using TB-IGRA was 89.4%, therefore TB-IGRA has diagnostic values in smear-negative pulmonary TB and extra-pulmonary TB diagnosis.Electronic supplementary materialThe online version of this article (doi:10.1186/s40249-017-0331-1) contains supplementary material, which is available to authorized users.

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Background: Shenxiong Glucose Injection (SGI) is a traditional Chinese medicine formula composed of ligustrazine hydrochloride and Danshen (Radix et rhizoma Salviae miltiorrhizae; Salvia miltiorrhiza Bunge, Lamiaceae). Our previous studies and others have shown that SGI has excellent therapeutic effects on myocardial ischemia (MI). However, the potential mechanisms of action have yet to be elucidated. This study aimed to explore the molecular mechanism of SGI in MI treatment.Methods: Sprague-Dawley rats were treated with isoproterenol (ISO) to establish the MI model. Electrocardiograms, hemodynamic parameters, echocardiograms, reactive oxygen species (ROS) levels, and serum concentrations of cardiac troponin I (cTnI) and cardiac troponin T (cTnT) were analyzed to explore the protective effect of SGI on MI. In addition, a model of oxidative damage and apoptosis in human umbilical vein endothelial cells (HUVECs) was established using CoCl2. Cell viability, Ca2+ concentration, mitochondrial membrane potential (MMP), apoptosis, intracellular ROS, and cell cycle parameters were detected in the HUVEC model. The expression of apoptosis-related proteins (Bcl-2, Caspase-3, PARP, cytoplasmic and mitochondrial Cyt-c and Bax, and p-ERK1/2) was determined by western blotting, and the expression of cleaved caspase-3 was analyzed by immunofluorescence.Results: SGI significantly reduced ROS production and serum concentrations of cTnI and cTnT, reversed ST-segment elevation, and attenuated the deterioration of left ventricular function in ISO-induced MI rats. In vitro, SGI treatment significantly inhibited intracellular ROS overexpression, Ca2+ influx, MMP disruption, and G2/M arrest in the cell cycle. Additionally, SGI treatment markedly upregulated the expression of anti-apoptotic protein Bcl-2 and downregulated the expression of pro-apoptotic proteins p-ERK1/2, mitochondrial Bax, cytoplasmic Cyt-c, cleaved caspase-3, and PARP.Conclusion: SGI could improve MI by inhibiting the oxidative stress and apoptosis signaling pathways. These findings provide evidence to explain the pharmacological action and underlying molecular mechanisms of SGI in the treatment of MI.

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