The regulatory effect of oxymatrine on the TLR4/MyD88/NF-κB signaling pathway in lipopolysaccharide-induced MS1 cells

Background Oxymatrine (OM), a major quinolizidine alkaloid extracted from the roots of Sophora flavescens, has been proved to regulate a variety of signaling pathways to produce a wide range of pharmacological effects. Objectives The regulatory effects of OM on the TLR4/MyD88/NF-κB signaling pathway under the stimulation of lipopolysaccharide (LPS) in MS1 cells were explored to illuminate the potential anti-inflammatory mechanism of OM for pancreatitis treatment. Methods The signaling molecules related to the TLR4/MyD88/NF-κB pathway in MS1 cells were detected by Western blotting under different conditions, including OM pretreatment and LPS stimulation. The mRNA expression levels of TLR4, MyD88, NF-κB p65 and IκBα were detected by real-time PCR. The NF-κB p65 nuclear translocation in MS1 cells was measured by immunofluorescence, and the pro-inflammatory cytokine of IL-1β was detected by ELISA. Results Increased levels of TLR4, MyD88 and NF-κB p65, induced by LPS stimulation, were significantly inhibited by OM pretreatment in MS1 cells. The decreased protein, but not mRNA, level of IκBα induced by LPS stimulation was increased by OM pretreatment. Meanwhile, LPS induced NF-κB p65 protein translocation to the nucleus as well as LPS increased expression of IL-1β were also inhibited by OM pretreatment. Conclusion Inhibitory effects of OM on molecules related to the TLR4/MyD88/NF-κB signaling pathway in pancreatic microvascular endothelial cells can alleviate inflammatory responses.