The Effects Of Toll-like Receptor3on Viability,Insulin Secretion Of NIT-1Cells

BackgroundsIn recent years, a large number of studies have shown that type1and type2diabetes blood glucose levels and insulin resistance index areclosely related to overactive by Toll-like receptors (TLRs),speculated thatit plays an important role in type1diabetes and type2diabetes in β-cellfailure.Toll-like receptors is a pattern recognition receptor,widely distributed in various cells such as polymerphonuclear cells, macrophages, lym-phocytes, etc. TLRs could be recognize the pathogen-associated molecul-ar patterns (PAMP), and activation of the body’s natural immune systemacquired immune system, inducing a variety of inflammatory cytokinerelease, resulting in autoimmune diseases.Now, at least13TLRs have been found in mammals. TLR3plays animportant role in the body’s antiviral immunity, it identifies the source ofthe virus dsRNA and its analogues as polyinosinic polycytidylic acid(PIC)to induce antiviral effect, but also can injury the body’s own immunefunction. It is reported that TLR3activation can significantly inhibit theproliferation of endothelial cells, however, affect the activation of TLR3islet β cell proliferation and biological function is unclear. ObjectiveWith mouse pancreatic β cell line (NIT-1) for the study, to explorethe effects of polyinosinic-polycytidylic acid on viability, inflammatorycytokine secretion and insulin secretion of NIT-1cells.MethodsWith mouse pancreaticβcell line NIT-1for the study，first usinginsulin release test to identify pancreatic β-cell function, then weredivided into different concentrations PIC (0.1,1,10ug/ml) treated groupand the control group, the following indicators to detect:21. The viability of NIT-1cells was detected by CCK8method;2. The cytokines(IL-1β,IL-6and TNF-α) was detected by ELISA;3. The insulin secretion of NIT-1cells was determined by glucosestimulated insulin secretion（GSIS）.Results1. NIT-1Cell lines showed good and growth polygon, pancreaticβ-cell activity is better;2. Compared with the control group, the viability of NIT-1cells wasinhibited in a dose-dependent manner after treatment with0.1,1and10ug/L PIC(P<0.05);3. Compared with the control group, the inflammatory cytokinesecretion was significantly increased after treatment with0.1,1and 10ug/L PIC(P<0.05);4. Compared with the control group, the insulin secretion of NIT-1cells was significantly decreased after treatment with0.1,1and10ug/LPIC(P<0.05）.ConclusionThe viability and insulin secretion of NIT-1cells is inhibited byinflammatory cytokines secretion after treatment with PIC of certainconcentrations．...