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首页> 外文期刊>Molecular medicine reports >Lipopolysaccharide-induced apoptosis in a murine intestinal endocrine cell line by modulation of Bcl-2, Bax and caspase-3
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Lipopolysaccharide-induced apoptosis in a murine intestinal endocrine cell line by modulation of Bcl-2, Bax and caspase-3

机译:脂多糖通过调节Bcl-2,Bax和caspase-3诱导小鼠肠道内分泌细胞凋亡

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Numerous studies have focused on how to modulate the secretion of glucagon-like peptide 1 (GLP-1) due to its marked anti-diabetic function. However, few studies have investigated the apoptosis of enteroendocrine L cells, which secrete GLP-1. The aim of this study was to determine whether lipopolysaccharide (LPS), a gut bacterial product, is capable of inducing apoptosis in the intestinal endocrine cell line STC-1. We found that LPS is capable of reducing the viability of STC-1 cells in a concentration-dependent manner. annexin V/propidium iodide (PI) double staining detected by fluorescence microscopy and flow cytometry revealed a strong apoptosis-inducing ability for LPS in STC-1 cells. Furthermore, western blotting revealed that exposure to LPS significantly decreased the expression of Bcl-2 and increased the expression of Bax and caspase-3. In conclusion, LPS induced the apoptosis of STC-1 cells in a dose-dependent manner, which may be responsible for the reduced secretion of GLP-1 in diabetes.
机译:由于其显着的抗糖尿病功能,许多研究集中在如何调节胰高血糖素样肽1(GLP-1)的分泌上。但是,很少有研究调查分泌GLP-1的肠内分泌L细胞的凋亡。这项研究的目的是确定一种肠道细菌产品脂多糖(LPS)是否能够诱导肠内分泌细胞系STC-1凋亡。我们发现LPS能够以浓度依赖的方式降低STC-1细胞的活力。通过荧光显微镜和流式细胞术检测到的膜联蛋白V /碘化丙啶(PI)双重染色显示,STC-1细胞中LPS具有很强的凋亡诱导能力。此外,蛋白质印迹显示暴露于LPS显着降低了Bcl-2的表达并增加了Bax和caspase-3的表达。总之,LPS以剂量依赖的方式诱导了STC-1细胞的凋亡,这可能是糖尿病中GLP-1分泌减少的原因。

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