白藜芦醇通过调节超氧化物歧化酶 1(SOD1)、谷胱甘肽过氧化物酶 1(GPx1)和 NADPH 氧化酶亚基(Nox4)的基因表达来减少内皮细胞的氧化应激。

Resveratrol reduces endothelial oxidative stress by modulating the gene expression of superoxide dismutase 1 (SOD1), glutathione peroxidase 1 (GPx1) and NADPH oxidase subunit (Nox4).

机构信息

Department of Pharmacology, Johannes Gutenberg University, Mainz, Germany.

出版信息

J Physiol Pharmacol. 2009 Oct;60 Suppl 4:111-6.

DOI:
Abstract

Resveratrol, an important antioxidant found in grapes and wine, is likely to contribute to red wine's potential to prevent human cardiovascular disease. In addition to its known (direct) antioxidant effect, we have found that resveratrol also regulates the gene expression of pro-oxidative and anti-oxidative enzymes in human endothelial cells. NADPH oxidases (Nox) are the predominant producers of superoxide in the vasculature, whereas superoxide dismutase (SOD) and glutathione peroxidase 1 (GPx1) are the major enzymes responsible for the inactivation of superoxide and hydrogen peroxide, respectively. Incubation of human umbilical vein endothelial cells (HUVEC) and HUVEC-derived EA.hy 926 cells with resveratrol resulted in a concentration- and time-dependent downregulation of Nox4, the most abundant NADPH oxidase catalytic subunit (quantitative real-time RT-PCR). The same resveratrol regimen upregulated the mRNA expression of SOD1 and GPx1. The addition the protein levels of SOD1 and GPx1 were enhanced by resveratrol in a concentration-dependent manner (Western blot analyses). Pretreatment of EA.hy 926 cells with resveratrol completely abolished DMNQ-induced oxidative stress. Thus, the expressional suppression of pro-oxidative genes (such as NADPH oxidase) and induction of anti-oxidative enzymes (such as SOD1 and GPx1) might be an important component of the vascular protective effect of resveratrol.

摘要

白藜芦醇是葡萄和葡萄酒中一种重要的抗氧化剂,可能有助于解释红葡萄酒预防人类心血管疾病的潜在机制。除了其已知的(直接)抗氧化作用外,我们还发现白藜芦醇还调节了人内皮细胞中促氧化和抗氧化酶的基因表达。NADPH 氧化酶(Nox)是血管中产生超氧阴离子的主要酶,而超氧化物歧化酶(SOD)和谷胱甘肽过氧化物酶 1(GPx1)分别是超氧阴离子和过氧化氢失活的主要酶。用白藜芦醇孵育人脐静脉内皮细胞(HUVEC)和 HUVEC 衍生的 EA.hy 926 细胞,导致 Nox4(最丰富的 NADPH 氧化酶催化亚基)的浓度和时间依赖性下调(定量实时 RT-PCR)。相同的白藜芦醇方案上调了 SOD1 和 GPx1 的 mRNA 表达。白藜芦醇以浓度依赖性方式增强 SOD1 和 GPx1 的蛋白水平(Western blot 分析)。用白藜芦醇预处理 EA.hy 926 细胞可完全消除 DMNQ 诱导的氧化应激。因此,促氧化基因(如 NADPH 氧化酶)的表达抑制和抗氧化酶(如 SOD1 和 GPx1)的诱导可能是白藜芦醇血管保护作用的一个重要组成部分。

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