脂多糖通过X盒结合蛋白1调节脂肪细胞胰岛素信号通路的机制
Mechanism of -lipopolysaccharide in regulating the insulin signaling pathway in adipocytes via X-box binding protein 1.
作者信息
Lu Jiayi, Wu Qianqi, Chen Yiyan, Ye Leilei, Su Yuan
机构信息
Stomatology Center, Shunde Hospital, Southern Medical University (The First People,s Hospital of Shunde), Shunde 528300, China.
Dept. of Periodontology, Stomatological Hospital, Southern Medical University, Guangzhou 510280, China.
出版信息
Hua Xi Kou Qiang Yi Xue Za Zhi. 2022 Mar 25;40(2):148-154. doi: 10.7518/hxkq.2022.02.004.
OBJECTIVES
This study aims to investigate the effect of X-box binding protein 1 (XBP1), a key signal molecule of ERS, on the insulin signaling pathway in adipocytes stimulated by ()-lipopolysaccharide (LPS), a pathogenic bacterium of periodontitis.
METHODS
Primary cultured rat adipocytes were stimulated by -LPS (100 ng·mL) for 4, 8, 12, and 24 h. The protein expression levels of insulin receptor substrate-1 (IRS-1), phosphoinositide dependent protein kinase (p-PDK-1), and protein kinase B (p-AKT-1) in the insulin signaling pathway were detected by Western blot analysis. pLVX-NC1, pLVX-XBP1, pLVX-NC2, and pLVX-XBP1-RNAi were transfected into adipocytes, respectively. The transfected rat adipocytes were stimulated by -LPS, and the protein expression of the insulin signaling pathway was detected by Western blot.
RESULTS
The Western Blot showed decreased protein expression of the insulin signaling pathway in rat adipocytes stimulated with -LPS compared with the control, and the difference was statistically significant (<0.05). The protein expression levels of IRS-1, p-PDK-1, and p-AKT in the rat adipocytes of pLVX-XBP1 were significantly higher than those in pLVX-NC1 at 8 and 12 h after -LPS stimulation (<0.05). The protein expression levels of IRS-1, p-PDK-1, and p-AKT in the rat adipocytes of pLVX-XBP1-RNAi were significantly lower than those in pLVX-NC2 at 4, 8, 12, and 24 h after -LPS stimulation (<0.05).
CONCLUSIONS
-LPS regulates the insulin signaling pathway in adipocytes th-rough XBP1.
目的
本研究旨在探讨内质网应激关键信号分子X盒结合蛋白1（XBP1）对牙周炎病原菌（）-脂多糖（LPS）刺激的脂肪细胞胰岛素信号通路的影响。
方法
原代培养的大鼠脂肪细胞用-LPS（100 ng·mL）刺激4、8、12和24小时。采用蛋白质免疫印迹分析检测胰岛素信号通路中胰岛素受体底物-1（IRS-1）、磷酸肌醇依赖性蛋白激酶（p-PDK-1）和蛋白激酶B（p-AKT-1）的蛋白表达水平。分别将pLVX-NC1、pLVX-XBP1、pLVX-NC2和pLVX-XBP1-RNAi转染到脂肪细胞中。对转染后的大鼠脂肪细胞进行-LPS刺激，采用蛋白质免疫印迹法检测胰岛素信号通路的蛋白表达。
结果
蛋白质免疫印迹结果显示，与对照组相比，-LPS刺激的大鼠脂肪细胞胰岛素信号通路蛋白表达降低，差异有统计学意义（<0.05）。-LPS刺激后8和12小时，pLVX-XBP1组大鼠脂肪细胞中IRS-1、p-PDK-1和p-AKT的蛋白表达水平显著高于pLVX-NC1组（<0.05）。-LPS刺激后4、8、12和24小时，pLVX-XBP1-RNAi组大鼠脂肪细胞中IRS-1、p-PDK-1和p-AKT的蛋白表达水平显著低于pLVX-NC2组（<0.05）。
结论
-LPS通过XBP1调节脂肪细胞中的胰岛素信号通路。
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