血管紧张素1-7降低脂肪细胞氧化应激增加脂联素表达

doi:10.3969/j.issn.1006-7795.2014.01.011

首都医科大学学报 ›› 2014, Vol. 35 ›› Issue (1): 45-50.doi: 10.3969/j.issn.1006-7795.2014.01.011

血管紧张素1-7降低脂肪细胞氧化应激增加脂联素表达

刘畅, 曹曦, 杨芳远, 张雪莲, 袁明霞, 杨金奎

首都医科大学附属北京同仁医院内分泌科, 北京 100730

收稿日期:2013-11-27 出版日期:2014-02-21 发布日期:2014-02-21
通讯作者: 杨金奎 E-mail:jinkui.yang@gmail.com
基金资助:
国家自然科学基金（81070644，81270918，81370946，81300726）；北京市自然科学基金（7131005）。

Effects of angiotensin-(1-7) on oxidative stress and adiponectin in adipocytes

Liu Chang, Cao Xi, Yang Fangyuan, Zhang Xuelian, Yuan Mingxia, Yang Jinkui

Department of Endocrinology, Beijing Tongren Hospital, Capital Medical University, Beijing 100730, China

Received:2013-11-27 Online:2014-02-21 Published:2014-02-21
Supported by:
This study was supported by the National Natural Science Foundation of China (81070644, 81270918, 81370946, 81300726);Natural Science Foundation of Beijing(7131005).

摘要/Abstract

摘要：

目的研究血管紧张素（1-7）[Ang-（1-7）]/Mas轴对于高糖培养脂肪细胞氧化应激及脂联素表达的作用。方法用前脂肪细胞株3T3L1诱导分化成成熟细胞，分别在培养基中加入外源性的Ang-（1-7） 10^-9mol/L，Mas受体抑制剂A779 10^-6mol/L，同时加入Ang-（1-7）及A779。分别用DHE荧光探针通过流式细胞术及用NBT染色法检测脂肪细胞内活性氧（ROS）含量。实时定量PCR方法检测脂联素及炎性反应因子的表达。无血清培养基培养脂肪细胞2 h后分别加入葡萄糖氧化酶（GO）50 mU/mL、100 mU/mL作用12 h建立氧化应激模型，研究Ang-（1-7）对于脂肪细胞氧化应激的作用及对脂联素表达的影响。结果 1Ang-（1-7）通过Mas受体降低脂肪细胞活性氧的产生。Mas受体抑制剂A779可逆转此作用。2构建氧化应激模型，脂肪细胞中的脂联素表达水平随着葡萄糖氧化酶浓度的增高而减少。3加入Ang-（1-7）可以逆转氧化应激导致的脂联素表达降低，抑制剂A779可以对抗Ang-（1-7）的这一作用。4Ang-（1-7）对于白细胞介素-6（IL-6）和肿瘤坏死因子-α（TNF-α）的mRNA表达水平没有影响。结论 Ang-（1-7）/Mas轴可以减少氧化应激产生的活性氧水平。Ang-（1-7）/Mas轴对氧化应激的保护作用可以增加抗胰岛素抵抗因子脂联素的表达。

关键词: 血管紧张素(1-7), A779, 氧化应激, 脂联素

Abstract:

Objective Although reactive oxygen species (ROS) contribute to glucose intolerance induced by the renin-angiotensin system (RAS) is well documented, the role of the newly discovered pathway of RAS, angiotensin Ang-(1-7)/Mas axis, in this process remains unknown. Here, we examined the effect of Ang-(1-7) on oxidative stress and adiponectin in adipocytes. Methods We treated fully differentiated 3T3-L1 cells with exogenous Ang-(1-7) to clarify its effects on ROS production. Intracellular ROS was measured by flow cytometry using dihydroethidium (DHE), and nitroblue tetrazolium assay. The cells were cultured in serum-free medium for 2 hours and added with glucose oxidase 50 mU/mL or 100 mU/mL for 12 hours to establish the oxidative stress model. We used these models to detect the role of Ang-(1-7) in oxidative stress of adipocytes. ROS production was slightly but significantly decreased in adipocytes treated with Ang-(1-7). Additionally, Mas receptor antagonist D-Ala7-Ang-(1-7) (A779) reversed the effect of Ang-(1-7) on oxidative stress. Furthermore, we also found that oxidative stress induced by glucose oxidase suppressed expression of adiponectin, an insulin-sensitive protein. However, the suppression of oxidative stress by Ang-(1-7) restored adiponectin expression, while A779 antagonize these changes induced by Ang-(1-7). Conclusion Ang-(1-7) can protect against oxidative stress and increase adiponectin expression in adipocytes. Ang-(1-7) may be a novel target for the improvement of insulin sensitivity by preventing oxidative stress.

Key words: angiotensin-(1-7), A779, oxidative stress, adiponectin

中图分类号:

R587.1

刘畅, 曹曦, 杨芳远, 张雪莲, 袁明霞, 杨金奎. 血管紧张素1-7降低脂肪细胞氧化应激增加脂联素表达[J]. 首都医科大学学报, 2014, 35(1): 45-50.

Liu Chang, Cao Xi, Yang Fangyuan, Zhang Xuelian, Yuan Mingxia, Yang Jinkui. Effects of angiotensin-(1-7) on oxidative stress and adiponectin in adipocytes[J]. Journal of Capital Medical University, 2014, 35(1): 45-50.

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血管紧张素1-7降低脂肪细胞氧化应激增加脂联素表达

Effects of angiotensin-(1-7) on oxidative stress and adiponectin in adipocytes

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