Total polyphenol of A nemarrhena asphodeloides ameliorates advanced glycation end products‐induced endothelial dysfunction by regulation of AMP ‐ K inase (知母多酚通过激活AMP‐激酶来缓解糖基化终末产物引起的内皮损伤)

作者：Qianwen Zhao, Yan Sun, Yu Ji, L. Xu, Kang Liu, Baolin Liu, Fang Huang · 发表于：Journal of Diabetes · 年份：2013 · DOI：10.1111/1753-0407.12111 · 被引用次数：10 · 研究领域：Advanced Glycation End Products research、Seaweed-derived Bioactive Compounds、Adipokines, Inflammation, and Metabolic Diseases

OBJECTIVE: Anemarrhena asphodeloides Bunge is widely used in China for the treatment of diabetes and the polyphenol components are responsible for its anti-diabetic action. This study aimed to investigate the effect of total polyphenol of Anemarrhena asphodeloides (TPAA) on endothelial dysfunction and to elucidate underlying mechanisms. METHODS: We stimulated endothelial cells with advanced glycation end products (AGEs) to establish the model of endothelial dysfunction in vitro and observed the effect of TPAA (10, 30, or 100 μg/mL) on AMP-Kinase (AMPK) activation implicated in regulation of nitric oxide (NO) and endothelin-1 (ET-1) production. Meanwhile, nuclear factor-κB (NF-κB) activation, intracellular reactive oxygen species (ROS) production, mitochondrial membrane potential (ΔΨm) and eNOS expression were investigated by western blot, fluorescence microscopy and real time-quantitative PCR analysis, respectively. RESULTS: Total polyphenol of Anemarrhena asphodeloides enhanced AMPK phosphorylation and promoted the basal NO production along with the inhibition of ET-1 secretion in endothelial cells. TPAA inhibited NF-κB activation by attenuating p65 phosphorylation and suppressed ROS production, well demonstrating its action in inhibition of ROS-associated inflammation in the endothelium. Meanwhile, TPAA protected mitochondrial function and endothelial homeostasis against AGEs insult by restoring ΔΨm and mRNA expression of eNOS. AGEs stimulation inhibited AMPK activation and...