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沙棘原花青素对人脐静脉内皮细胞氧化损伤的调控作用

Regulatory Effect of Sea-Buckthorn Procyanidins on Oxidative Injury HUVECs.

作者信息

Lin Ximeng, Yuen Michael, Yuen Tina, Yuen Hywel, Wang Min, Peng Qiang

机构信息

College of Food Science and Engineering, Northwest A&F University, Yangling, China.

Puredia Limited, Xining, China.

出版信息

Front Nutr. 2022 May 17;9:850076. doi: 10.3389/fnut.2022.850076. eCollection 2022.

Abstract

As society develops and aging populations increase, the incidence of arteriosclerosis, a seriously harmful cardiovascular disease (CVD) which mostly results from endothelial cellular oxidative damage, has continuously risen. Procyanidins from sea-buckthorn is a powerful antioxidant, although its protective effect on the cardiovascular system is not yet clearly understand. In this study, oxidative damaged HUVECs induced by palmitate acid (PA) were used as a model and the regulatory effect of procyanidins from sea-buckthorn (SBP) on HUVECs were investigated. The results showed SBP can be used for 12 h by HUVECs and had no detective cytotoxicity to them under 400 μg/L. Also, different concentrations of SBP can increase mitochondrial membrane potential and NO level and decrease LDH leakage in a dose-effect relationship, indicating SBP can improve oxidative damage. In addition, western blots and qPCR results showed SBP regulation on oxidative injured HUVECs is probably through p38MAPK/NF-κB signal pathway. This study revealed the molecular mechanism of procyanidins in decreasing endothelial oxidative damage, providing a theoretical foundation for further research on natural bioactive compounds to exert antioxidant activity in the body and prevent and improve cardiovascular diseases.

摘要

随着社会发展和老龄化人口增加,动脉硬化这种主要由内皮细胞氧化损伤导致的严重有害心血管疾病(CVD)的发病率持续上升。沙棘原花青素是一种强大的抗氧化剂,尽管其对心血管系统的保护作用尚未完全明确。本研究以棕榈酸(PA)诱导的氧化损伤人脐静脉内皮细胞(HUVECs)为模型,研究了沙棘原花青素(SBP)对HUVECs的调节作用。结果表明,HUVECs可利用SBP 12小时,且在400μg/L以下对其无明显细胞毒性。此外,不同浓度的SBP能以剂量效应关系增加线粒体膜电位和一氧化氮(NO)水平,并降低乳酸脱氢酶(LDH)泄漏,表明SBP能改善氧化损伤。另外,蛋白质免疫印迹法(western blots)和实时荧光定量聚合酶链反应(qPCR)结果显示,SBP对氧化损伤的HUVECs的调节可能是通过p38丝裂原活化蛋白激酶/核因子κB(p38MAPK/NF-κB)信号通路。本研究揭示了原花青素减少内皮氧化损伤的分子机制,为进一步研究天然生物活性化合物在体内发挥抗氧化活性以及预防和改善心血管疾病提供了理论基础。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/8d00/9152354/ef90c427398a/fnut-09-850076-g0001.jpg

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