中文摘要：

血浆 lipopolysaccharide ( LPS )的增加的层次在肥胖和糖尿病 patients.This 学习被发现了的背景是在胰腺的贝它房间生存能力和 caspase 的参与上调查 LPS 的效果 3 在显示的时间与 LPS 在 NIT-1 房间 line.Methods 老鼠 insulinoma NIT-1 房间被对待， dose.Cell 生存能力被测量由数 kit-8 象reagent.Toll一样受体 4 的房间( TLR4 )， caspase 3 并且劈开的 caspase 3 被西方的 blotting.Insulin 检测决定

英文摘要：

Background Increased levels of plasma lipopolysaccharide （LPS） have been found in obesity and diabetes patients. This study was to investigate the effect of LPS on pancreatic beta-cell viability and the involvement of caspase 3 in NIT-1 cell line. Methods Mouse insulinoma NIT-1 cells were treated with LPS for the indicated time and dose. Cell viability was measured by cell counting kit-8 reagent. Toll-like receptor 4 （TLR4）, caspase 3 and cleaved caspase 3 were detected by Western blotting. Insulin was determined by radioimmunoassay （RIA）. Results LPS promoted NIT-1 cell proliferation at 1 μg/ml, peaked at 72 hours of incubation. A reduction in cleavage of caspase 3 was observed upon LPS treatment. Bay11-7082, a specific inhibitor of nuclear factor （NF）-κB, blunted LPS-induced inhibition of caspase 3 cleavage. Reduction in chronic insulin secretion was observed after treatment with LPS at 1 μg/ml for 48 and 72 hours, not for 24 hours. TLR4 protein was upregulated when NIT-1 cells were treated with LPS at 1 μg/ml for 24 hours. Conclusions LPS promotes early NIT-1 cell proliferation in association with NF-KB-mediated inhibition of caspase 3 cleavage. LPS exerts a time-dependent inhibitory effect on chronic insulin secretion from NIT-1 cells.