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白藜芦醇是红葡萄酒中的一种多酚化合物,可保护内皮细胞免受氧化型低密度脂蛋白诱导的细胞毒性作用。

Resveratrol, a polyphenolic compound in red wine, protects against oxidized LDL-induced cytotoxicity in endothelial cells.

作者信息

Ou Hsiu-Chung, Chou Fen-Pi, Sheen Huey-Min, Lin Tsung-Min, Yang Ching-Hwa, Huey-Herng Sheu Wayne

机构信息

Division of Endocrinology and Metabolism, Department of Education and Medical Research, Taichung Veterans General Hospital, No. 160, Sec. 3, Taichung-Kang Road, Taichung 407, Taiwan.

出版信息

Clin Chim Acta. 2006 Feb;364(1-2):196-204. doi: 10.1016/j.cccn.2005.06.018. Epub 2005 Aug 10.

Abstract

BACKGROUND

Resveratrol, a polyphenolic constituent of red wine, has antioxidant effects. However, its protective effects against oxLDL-induced endothelial injury remained unclarified.

METHODS

Primary human umbilical vein endothelial cell cultures (HUVECs) treated with oxLDL (200 microg/ml) were used to explore the protective effect of resveratrol. Cytotoxicity of oxLDL on HUVECs was studied by measuring lactate dehydrogenase (LDH) release, methylthiazol tetrazolium (MTT) and apoptotic cell death as characterized by terminal deoxynucleotidyl transferase-mediated dUTP nick end-labeling (TUNEL) stain. We also measured the production of reactive oxygen species (ROS) by using the fluorescnet probe 2', 7'-dichlorofluorescein acetoxymethyl ester (DCF-AM), and observed the activity of antioxidant enzymes. Furthermore, several apoptotic signaling pathway with increased cytosolic calcium, alteration of mitochondrial membrane potential, cytochrome c release and activation of caspase 3 were also investigated.

RESULTS

Resveratrol attenuated oxLDL-induced cytotoxicity, apoptotic features, generation of ROS and intracellular calcium accumulation. OxLDL-induced mitochondria membrane potential collapase, cytochrome c release and activation of caspase 3 in HUVECs were also suppressed by resveratrol pretreatment.

CONCLUSIONS

Red wine intake may protect against oxLDL-induced dysfunction of endothelial cells.

摘要

背景

白藜芦醇是红酒中的一种多酚成分,具有抗氧化作用。然而,其对氧化型低密度脂蛋白(oxLDL)诱导的内皮损伤的保护作用仍不明确。

方法

用oxLDL(200微克/毫升)处理的原代人脐静脉内皮细胞培养物(HUVECs)来探究白藜芦醇的保护作用。通过测量乳酸脱氢酶(LDH)释放、噻唑蓝(MTT)以及以末端脱氧核苷酸转移酶介导的dUTP缺口末端标记(TUNEL)染色为特征的凋亡细胞死亡,研究oxLDL对HUVECs的细胞毒性。我们还使用荧光探针2',7'-二氯荧光素乙酰甲酯(DCF-AM)测量活性氧(ROS)的产生,并观察抗氧化酶的活性。此外,还研究了几种凋亡信号通路,包括细胞溶质钙增加、线粒体膜电位改变、细胞色素c释放和半胱天冬酶3激活。

结果

白藜芦醇减轻了oxLDL诱导的细胞毒性、凋亡特征、ROS产生和细胞内钙积累。白藜芦醇预处理还抑制了oxLDL诱导的HUVECs线粒体膜电位崩溃、细胞色素c释放和半胱天冬酶3激活。

结论

饮用红酒可能预防oxLDL诱导的内皮细胞功能障碍。

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