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红景天苷可减轻高糖诱导的人脐静脉内皮细胞功能障碍。

Rhodiola crenulata Attenuates High Glucose Induced Endothelial Dysfunction in Human Umbilical Vein Endothelial Cells.

机构信息

* Graduate Institute of Medical Sciences, National Defense Medical Center, Taipei, Taiwan.

∥ Division of Cardiology, Department of Internal Medicine, Taoyuan Armed Forces General Hospital, Taoyuan, Taiwan.

出版信息

Am J Chin Med. 2017;45(6):1201-1216. doi: 10.1142/S0192415X17500665. Epub 2017 Aug 22.

Abstract

Rhodiola crenulata root extract (RCE), a traditional Chinese medicine, has been shown to regulate glucose and lipid metabolism via the AMPK pathway in high glucose (HG) conditions. However, the effect of RCE on HG-induced endothelial dysfunction remains unclear. The present study was designed to examine the effects and mechanisms of RCE against hyperglycemic insult in endothelial cells. Human umbilical vein endothelial cells (HUVECs) were pretreated with or without RCE and then exposed to 33[Formula: see text]mM HG medium. The cell viability, nitrite production, oxidative stress markers, and vasoactive factors, as well as the mechanisms underlying RCE action, were then investigated. We found that RCE significantly improved cell death, nitric oxide (NO) defects, and oxidative stress in HG conditions. In addition, RCE significantly decreased the HG-induced vasoactive markers, including endothelin-1 (ET-1), fibronectin, and vascular endothelial growth factor (VEGF). However, the RCE-restored AMPK-Akt-eNOS-NO axis and cell viability were abolished by the presence of an AMPK inhibitor. These findings suggested that the protective effects of RCE were associated with the AMPK-Akt-eNOS-NO signaling pathway. In conclusion, we showed that RCE protected endothelial cells from hyperglycemic insult and demonstrated its potential for use as a treatment for endothelial dysfunction in diabetes mellitus.

摘要

红景天根提取物(RCE)是一种传统中药,已被证明可通过 AMPK 途径调节高糖(HG)条件下的葡萄糖和脂质代谢。然而,RCE 对 HG 诱导的内皮功能障碍的影响尚不清楚。本研究旨在研究 RCE 对内皮细胞高糖损伤的作用及其机制。用人脐静脉内皮细胞(HUVEC)用或不用 RCE 预处理,然后暴露于 33[Formula: see text]mM HG 培养基中。然后研究细胞活力、亚硝酸盐产生、氧化应激标志物和血管活性因子,以及 RCE 作用的机制。我们发现,RCE 可显著改善 HG 条件下的细胞死亡、一氧化氮(NO)缺陷和氧化应激。此外,RCE 还显著降低了 HG 诱导的血管活性标志物,包括内皮素-1(ET-1)、纤维连接蛋白和血管内皮生长因子(VEGF)。然而,存在 AMPK 抑制剂会消除 RCE 恢复的 AMPK-Akt-eNOS-NO 轴和细胞活力。这些发现表明,RCE 的保护作用与 AMPK-Akt-eNOS-NO 信号通路有关。总之,我们表明 RCE 可保护内皮细胞免受高血糖损伤,并证明其在治疗糖尿病内皮功能障碍方面具有潜力。

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