Context: Oxymatrine (OMT) has various pharmacological effects, including immune reaction regulation, anti-inflammation and anti-hypersensitive reaction.Objective: This is the first report to investigate the molecular mechanism of OMT function in l-arginine (Arg)-induced acute pancreatitis (AP) involving intestinal injury.Materials and methods: Rat pancreatic AR42J and small intestinal IEC-6 cells were treated with Arg (200–800 µM) for 48 h plus OMT (4 mg/mL) treatment. Thirty adult Wistar rats were randomly assigned to control (saline), AP (i.p. of 250 mg/100 g body weight Arg) and OMT (i.p. injection of 50 mg/kg b.w. OMT every 6 h following Arg). Both cells and rats were harvested at 48 h.Results: Arg-induced cell proliferation in both rats AR42J (EC50 633.9 ± 31.4 µM) and IEC-6 cells (EC50 571.3 ± 40.4 µM) in a dose-dependent manner, which was significantly inhibited by OMT (4 mg/mL). Meanwhile, Arg (600 µM) induced expression of proinflammatory cytokines (TNF-α, IL-6, IL-1β, NF-κB, IL-17A/IL-17F and IFN-γ) and activation of p-p38/p-ERK in vitro, which was reversed by OMT. In vivo, OMT (50 mg/kg) inhibited 250 mg/100 g of Arg-induced AP involving intestinal injury, including inhibiting Arg-induced inflammatory in pancreas and intestine, inhibiting Arg-induced increase of TNF-α, IL-6, IL-1β, NF-κB and p-p38/p-ERK-MAPK signalling, and inhibiting Arg-induced increase of IL-17A/IL-17F, IFN-γ, ROR-γt and T-bet. Meanwhile, OMT inhibited Arg-induced expression of CD44 and CD55 in intestinal injury.Discussion and conclusions: OMT protects against Arg-induced AP involving intestinal injury via regulating Th1/Th17 cytokines and MAPK/NF-κB signalling, which is a promising therapeutic agent in clinics.

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HBV intrauterine infection was primarily due to peripheral blood mononuclear cell maternal-fetal transportation in the second trimester in pregnant women.

Apigenin is a flavonoid of low toxicity and multiple beneficial bioactivities, including the properties of antitumor, antioxidant, anti‐inflammatory, and antiviral activities. However, the effects of Apigenin on influenza virus infection remain poorly understood. Thus, the aim of this study is to investigate the effect of Apigenin on influenza A virus (IAV)‐induced inflammation and viral replication. This study demonstrated that Apigenin treatment significantly suppressed IAV‐induced upregulation of retinoic acid‐inducible gene‐I (RIG‐I) expression, as well as the production of proinflammatory cytokines and interferons (IFN‐β and IFN‐λ1). Meanwhile, Apigenin also protected cells from IAV‐induced cell death. In addition, Apigenin specifically inhibited the activation of RIG‐I signaling via promoting the ubiquitin‐mediated degradation of RIG‐I, which may cause by the disrupting its interaction with heat shock protein 90α. Interestingly, instead of enhancing viral replication due to the inhibitory effects of Apigenin on the activation of RIG‐I and expression of IFNs, Apigenin inhibited IAV replication in vitro. Further study demonstrated that Apigenin inhibited the influenza viral neuraminidase (NA) activity. Thus, Apigenin may serve as a promising supplementary approach for treatment of influenza because it protected cells from IAV‐induced cell death and inhibited viral NA activity to suppress viral replication.

BackgroundThe human heart consists of several cell types with distinct lineage origins. Interactions between these cardiac progenitors are very important for heart formation. The muscle segment homeobox gene family plays a key role in the cell morphogenesis and growth, controlled cellular proliferation, differentiation, and apoptosis, but the relationships between the genetic abnormalities and CHD phenotypes still remain largely unknown. The aim of this work was to evaluate variations in MSX1 and MSX2 for their possible associations with CHD.MethodsWe sequenced the MSX1 and MSX2 genes for 300 Chinese Han CHD patients and 400 normal controls and identified the variations. The statistical analyses were conducted using Chi-Square Tests as implemented in SPSS (version 19.0). The Hardy-Weinberg equilibrium test of the population was carried out using the online software OEGE.ResultsSix variations rs4647952, rs2048152, rs4242182, rs61739543, rs111542301 and rs3087539 were identified in the MSX2 gene, but the genetic heterozygosity of those SNPs was very low. In contrast, the genetic heterozygosity of two variations rs3821949 near the 5’UTR and rs12532 within 3’UTR of the MSX1 gene was considerably high. Statistical analyses showed that rs3821949 and rs12532 were associated with the risk of CHD (specifically VSD).ConclusionsThe SNPs rs3821949 and rs12532 in the MSX1 gene were associated with CHD in Chinese Han populations.