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

被引:15
作者
Huang, Li-Yen [1 ,6 ]
Yen, I-Chuan [2 ]
Tsai, Wei-Cheng [3 ]
Ahmetaj-Shala, Blerina [7 ]
Chang, Tsu-Chung [4 ]
Tsai, Chien-Sung [5 ,8 ,9 ]
Lee, Shih-Yu [1 ,3 ]
机构
[1] Natl Def Med Ctr, Grad Inst Med Sci, Taipei, Taiwan
[2] Natl Def Med Ctr, Sch Pharm, Taipei, Taiwan
[3] Natl Def Med Ctr, Grad Inst Aerosp & Undersea Med, POB 90048-514, Taipei 114, Taiwan
[4] Natl Def Med Ctr, Dept Biochem, Taipei, Taiwan
[5] Natl Def Med Ctr, Dept & Grad Inst Pharmacol, Taipei, Taiwan
[6] Taoyuan Armed Forces Gen Hosp, Div Cardiol, Dept Internal Med, Taoyuan, Taiwan
[7] Imperial Coll London, Natl Heart & Lung Inst, London, England
[8] Taoyuan Armed Gen Forces Gen Hosp, Dept Surg, Div Cardiovasc Surg, Taoyuan, Taiwan
[9] Triserv Gen Hosp, Dept Surg, Div Cardiovasc Surg, Taipei, Taiwan
来源
AMERICAN JOURNAL OF CHINESE MEDICINE | 2017年 / 45卷 / 06期
关键词
Rhodiola crenulata; High Glucose; Endothelial Dysfunction; AMPK; eNOS; ACTIVATED PROTEIN-KINASE; NITRIC-OXIDE SYNTHASE; INDUCED OXIDATIVE STRESS; NF-KAPPA-B; INDUCED APOPTOSIS; LIPID-METABOLISM; DISEASE; AMPK; PATHOGENESIS; FIBRONECTIN;
D O I
10.1142/S0192415X17500665
中图分类号
R [医药、卫生];
学科分类号
10 ;
摘要
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 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.
引用
收藏
页码:1201 / 1216
页数:16
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