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| 视黄醇类受体激动剂通过抑制人内皮细胞PKC（蛋白激酶C）活性拮抗高糖诱导的氧化应激 |
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| RXR agonists inhibit high-glucose-induced oxidative stress by repressing PKC activity in human endothelial cells |
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| Chai D., Wang B., Shen L., Pu J., Zhang X.-k., He B. 2009/5/29 18:38:57 |
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Free Radical Biology and Medicine, 2008, Volume 44, Issue 7
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| Activation of retinoid X receptor (RXR) is known to exert antiatherogenic effects. However, the underlying mechanism remains unclear. In this study, we examined the effects of the RXR agonists 9-cis-retinoic acid and SR11237 on high-glucose-induced oxidative stress in human endothelial cells. Our results demonstrated that high-glucose-induced oxidative stress in human umbilical vein endothelial cells (HUVECs) was mainly mediated through its activation of the Nox4, gp91phox, and p22phox components of nicotinamide adenine dinucleotide phosphate oxidase. Treatment of endothelial cells with RXR agonists resulted in significant inhibition of high-glucose-induced oxidative stress and expression of Nox4, gp91phox, and p22phox. The effect of RXR agonists was due to their inhibition of Rac-1 activation. Furthermore, RXR agonists rapidly inhibited high-glucose-induced activation of protein kinase C (PKC), an upstream activator of Rac-1. To study whether the rapid inhibitory effects of RXR agonists were mediated by RXR, we examined the effect of RXR downregulation by RXR siRNA. Our results showed that expression of RXR siRNA largely abrogated the effects of RXR agonists, suggesting the requirement of RXR expression. Interestingly, RXRα, which was diffusely distributed in HUVECs, accumulated mainly in the nucleus upon high glucose exposure. Treatment of cells with RXR agonists prevented the effect of high glucose. Thus, RXR ligands rapidly inhibit high-glucose-induced oxidative stress by antagonizing high-glucose-induced PKC activation, and cytoplasmic RXRα is implicated in this regulation. © 2007 Elsevier Inc. All rights reserved. |
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| Correspondence Address: Zhang, X.-k.; Institute for Biomedical Research, Xiamen University, Xiamen, China; email: xzhang@burnham.org |
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 疾病资源中心
王燕燕 王曙
上海交通大学附属瑞金医院内分泌科
患者，女，69岁。2009年1月无明显诱因下出现乏力，当时程度较轻，未予以重视。2009年3月患者乏力症状加重，尿色逐渐加深，大便习惯改变，颜色变淡。4月18日入我院感染科治疗，诉轻度头晕、心慌，体重减轻10kg。无肝区疼痛，无发热，无腹痛、腹泻、腹胀、里急后重，无恶性、呕吐等。入院半月前于外院就诊，查肝功能：ALT 601IU/L，AST 785IU/L，TBIL 97.7umol/L，白蛋白 41g/L，甲状腺功能：游离T3 30.6pmol/L，游离T4 51.9pmol/L，心电图示快速房颤。
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