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芍药苷对过氧化氢诱导的人脐静脉内皮细胞氧化应激的保护作用。

Protective effects of peoniflorin against hydrogen peroxide-induced oxidative stress in human umbilical vein endothelial cells.

机构信息

Department of Dermatovenereology, West China Hospital of Sichuan University, Chengdu, Sichuan Province, PR China.

出版信息

Can J Physiol Pharmacol. 2011 Jun;89(6):445-53. doi: 10.1139/y11-034. Epub 2011 Jul 21.

DOI:10.1139/y11-034
PMID:21777057
Abstract

Peoniflorin (PF), extracted from the root of Paeonia lactiflora Pall., has been reported to have anti-inflammation and antioxidant effects in several animal models. Herein, we investigated the protective effects of PF against hydrogen peroxide (H(2)O(2))-induced oxidative damage in human umbilical vein endothelial cells (HUVECs). HUVECs were treated by H(2)O(2) (240 µmol/L) with or without PF. PF significantly increased the percent cell viability of HUVECs injured by H(2)O(2) using the 3-(4,5-dimethylthiazol-2-yl)-2,5-diphenyl tetrazolium bromide (MTT) assay. By flow cytometric analysis, PF markedly attenuated H(2)O(2)-induced apoptosis and intracellular reactive oxygen species production. In addition, PF also displayed a dose-dependent reduction of lactate dehydrogenase leakage, malondialdehyde formation, and caspase-3 proteolytic activities in H(2)O(2)-treated cells, which was accompanied with a restoration of the activities of endogenous antioxidants, including total superoxide dismutase and glutathione peroxidase. Finally, Western blot data revealed that H(2)O(2) upregulated phosphorylation of extracellular signal-regulated kinase 1/2 in HUVECs, which was almost completely reversed by PF. Taken together, our data provide the first evidence that PF has a protective ability against oxidative damage in HUVECs. PF may be a candidate medicine for the treatment of vascular diseases associated with oxidative stress.

摘要

芍药苷(PF)从芍药的根中提取,据报道在几种动物模型中具有抗炎和抗氧化作用。在此,我们研究了 PF 对人脐静脉内皮细胞(HUVEC)中过氧化氢(H2O2)诱导的氧化损伤的保护作用。用 H2O2(240µmol/L)处理 HUVEC 并加入或不加入 PF。MTT 法检测表明 PF 可显著提高 H2O2 损伤的 HUVEC 的细胞存活率。通过流式细胞术分析,PF 明显减弱了 H2O2 诱导的细胞凋亡和细胞内活性氧的产生。此外,PF 还显示出剂量依赖性降低了 H2O2 处理细胞中的乳酸脱氢酶漏出、丙二醛形成和半胱氨酸天冬氨酸蛋白酶-3 的蛋白水解活性,同时恢复了内源性抗氧化剂的活性,包括总超氧化物歧化酶和谷胱甘肽过氧化物酶。最后,Western blot 数据表明 H2O2 可使 HUVEC 中细胞外信号调节激酶 1/2 的磷酸化增加,而 PF 几乎完全逆转了这一作用。总之,我们的数据首次提供了 PF 对 HUVEC 氧化损伤具有保护能力的证据。PF 可能是治疗与氧化应激相关的血管疾病的候选药物。

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