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高糖通过增加氧化应激和诱导血管平滑肌细胞核因子-κB激活来抑制ABCG1表达

[High glucose suppresses ABCG1 expression by increasing oxidative stress and inducing nuclear factor-kappaB activation in vascular smooth muscle cells].

作者信息

Xue Jia-Hong, Yuan Zu-Yi, Wu Yue, Zhao Yan

机构信息

Department of Cardiovascular Medicine, First Affiliated Hospital, Key Laboratory of Environment and Gene Related Disease of Ministry Education, Xi'an Jiaotong University College of Medicine, Xi'an 710061, China.

出版信息

Nan Fang Yi Ke Da Xue Xue Bao. 2008 Jun;28(6):933-7.

PMID:18583231
Abstract

OBJECTIVE

To investigate the role of high glucose in the expression of ATP-binding cassette (ABC) transporters A1 (ABCA1) and G1 (ABCG1) in human vascular smooth muscle cells (VSMCs) and its possible mechanisms.

METHODS

VSMCs were incubated in the presence of glucose at the concentrations ranging from 5 to 30 mmol/L for 1 to 7 days, and real-time PCR and Western blotting were used to measure the mRNA and protein expressions of ABCA1 and ABCG1. The effects of cells pretreatment with antioxidant NAC (10 mmol/L) and nuclear factor-kappaB (NF-kappaB) inhibitors BAY 11-7085 (10 micromol/L) and TPCK (10 micromol/L) were also tested on ABCA1 and ABCG1 expressions.

RESULTS

High glucose suppressed, in a time- and dose-dependent manner, ABCG1 expression in incubated human VSMCs, and this effect was abolished by pretreatment with the antioxidant and nuclear factor-kappaB (NF-kappaB) inhibitors, but ABCA1 expression was not significantly decreased in the presence of high glucose.

CONCLUSION

High glucose suppresses ABCG1 expression in human VSMCs possibly due to increased oxidative stress and NF-kappaB activation induced by high glucose.

摘要

目的

探讨高糖对人血管平滑肌细胞(VSMCs)中ATP结合盒转运蛋白A1(ABCA1)和G1(ABCG1)表达的影响及其可能机制。

方法

将VSMCs置于浓度为5至30 mmol/L的葡萄糖环境中孵育1至7天,采用实时定量PCR和蛋白质印迹法检测ABCA1和ABCG1的mRNA及蛋白表达。同时检测抗氧化剂NAC(10 mmol/L)、核因子-κB(NF-κB)抑制剂BAY 11-7085(10 μmol/L)和TPCK(10 μmol/L)预处理细胞对ABCA1和ABCG1表达的影响。

结果

高糖以时间和剂量依赖的方式抑制人VSMCs中ABCG1的表达,抗氧化剂和NF-κB抑制剂预处理可消除该作用,但高糖存在时ABCA1表达无明显降低。

结论

高糖可能通过增加氧化应激及激活NF-κB抑制人VSMCs中ABCG1的表达。

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