碧萝芷通过激活蛋白激酶B改善AML12细胞胰岛素抵抗

doi:10.12007/j.issn.0258-4646.2020.01.004

科研成果详情

题名	碧萝芷通过激活蛋白激酶B改善AML12细胞胰岛素抵抗
其他题名	Pycnogenol improves insulin resistance by activating AKT expression in AML12 cells
作者	钟文霞 1; 王艺颖1,2; 范斌 3; 谷剑秋 1
发表日期	2019
发表期刊	中国医科大学学报影响因子和分区
语种	中文
原始文献类型	学术期刊
关键词	碧萝芷胰岛素抵抗糖异生糖酵解
摘要	目的探讨碧萝芷(PYC)对油酸(OA)诱导的AML12细胞胰岛素抵抗的作用及其相关分子机制。方法将细胞分为空白对照组、PYC50 (50μg/mL)组、OA (200μmol/L)组、PYC10 (10μg/mL)+OA (200μmol/L)组、PYC50 (50μg/mL)+OA (200μmol/L)组。应用葡萄糖氧化酶法检测葡萄糖摄取量,糖原染色法检测糖原含量。实时PCR检测糖异生基因G6PC、PEPCK、PGC1αmRNA和糖酵解基因Eno1、PKLR、Gpi1 mRNA表达,Western blotting检测IRS/p-IRS、AKT/p-AKT、p-GSK3β的表达。结果与OA组比较,PYC10+OA组、PYC50+OA组培养基上清葡萄糖剩余含量明显减少(P <0.05),糖原含量明显增加(P <0.05)。PYC10+OA组、PYC50+OA组分别与OA组比较,糖异生基因G6PC、PEPCK、PGC1αmRNA表达无统计学差异(P> 0.05),糖酵解基因Eno1、Gpi1mRNA表达无统计学差异(P> 0.05),但PKLR mRNA表达增加(P <0.05)。在胰岛素信号通路中,PYC10+OA组、PYC50+OA组分别与OA组比较,p-IRS表达无统计学差异(P> 0.05),但p-AKT、p-GSK3β蛋白表达明显升高(P <0.05)。结论 PYC通过激活AKT促进PKLR表达增加糖酵解,并且促进p-GSK3β表达增加糖原合成来调控AML12细胞胰岛素抵抗。
其他摘要	Objective To investigate the protective effect of pycnogenol(PYC) on oleic acid(OA) -induced insulin resistance in AML12 cells and its underlying mechanisms of action. Methods AML12 cells were divided into the blank control group,PYC50(50 μg/mL) group,OA(200 μmol/L) group,PYC10(10 μg/mL) +OA(200 μmol/L) group,and PYC50(50 μg/mL) +OA(200 μmol/L) group. Glucose uptake was examined using the glucose oxidase assay,and glycogen content was detected by PAS staining. The mRNA expression of the genes involved in gluconeogenesis(G6PC,PEPCK,and PGC1α) and glycolysis(Eno1,PKLR,and Gpi1) was detected by real time-PCR. The levels of proteins involved in the insulin signaling pathway(IRS/p-IRS,AKT/p-AKT,and p-GSK3β) were detected by Western blotting. Results The residual glucose content was significantly decreased(P < 0.05) and the glycogen content was significantly increased in the PYC10+OA and PYC50+OA groups compared to the OA group(P < 0.05) . In comparison to the OA group,there was no significant difference in the expression of G6PC,PEPCK,PGC1α,Eno1,and Gpi1 mRNA(P > 0.05),while PKLR mRNA expression was significantly increased(P < 0.05) in the PYC10+OA and PYC50+OA groups. Analysis of insulin signaling pathway activation revealed that the expression of p-IRS was unaltered in the PYC10+OA and PYC50+OA groups(P > 0.05),while the expression of p-AKT and p-GSK3β was significantly increased(P < 0.05) when compared to the OA group. Conclusion PYC increased the expression of PKLR and p-GSK3β by activating AKT,which further increased glycolysis and promoted glycogen synthesis,thus improving the OA-induced insulin resistance in AML12 cells.
资助项目	国家自然科学基金（81100216）
ISSN	0258-4646
卷号	49 期号:01 页码:16-20
DOI	10.12007/j.issn.0258-4646.2020.01.004
页数	5
收录类别	CNKI ; 万方 ; 维普 ; 北大核心 ; PKU ; CSCD ; ISTIC
学科领域	医药、卫生 ; 内科学
URL	查看原文
CSCD记录号	CSCD:6664911
CNKI分类号	R587.1
万方分类号	R587(内分泌腺疾病及代谢病)
引用统计
文献类型	期刊论文
条目标识符	https://kms.wmu.edu.cn/handle/3ETUA0LF/43606
专题	附属第二医院_营养科
作者单位	1.中国医科大学附属第一医院内分泌与代谢病科; 2.温州医科大学附属第二医院营养科; 3.中国医科大学附属盛京医院神经内科
推荐引用方式 GB/T 7714	钟文霞,王艺颖,范斌,等. 碧萝芷通过激活蛋白激酶B改善AML12细胞胰岛素抵抗[J]. 中国医科大学学报,2019,49(01):16-20.
APA	钟文霞, 王艺颖, 范斌, & 谷剑秋. (2019). 碧萝芷通过激活蛋白激酶B改善AML12细胞胰岛素抵抗. 中国医科大学学报, 49(01), 16-20.
MLA	钟文霞,et al."碧萝芷通过激活蛋白激酶B改善AML12细胞胰岛素抵抗".中国医科大学学报 49.01(2019):16-20.

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