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染井吉野樱通过激活 AMP 激活的蛋白激酶和磷脂酰肌醇 3-激酶/蛋白激酶 B 通路促进 L6 大鼠骨骼肌细胞葡萄糖摄取。

Prunus yedoensis Matsum. stimulates glucose uptake in L6 rat skeletal muscle cells by activating AMP-activated protein kinase and phosphatidylinositol 3-kinase/Akt pathways.

机构信息

Department of Biotechnology, College of Life Science and Biotechnology, Yonsei University, 262 Seongsanno, Seodaemun-gu, Seoul 120-749, Korea.

出版信息

Nat Prod Res. 2012;26(17):1610-5. doi: 10.1080/14786419.2011.574133. Epub 2011 Aug 2.

Abstract

Prunus yedoensis Matsum. is used as a medicinal plant to alleviate symptoms of diabetes; however, the molecular mechanism underlying its antihyperglycaemic activity is unknown. In this study, we investigated the antihyperglycaemic effects of P. yedoensis and its molecular mechanism. Prunus yedoensis leaf extract (PLE) increased the glucose uptake of phosphorylatinginsulin receptor substrate (IRS)-1, 3'-phosphoinositide-dependent kinase (PDK)-1 and Akt PLE, and also increased the phosphorylation of AMP-activated protein kinase (AMPK) and p38 mitogen-activated protein kinase (p38 MAPK). PLE-stimulated glucose uptake was blocked by an AMPK inhibitor (Compound C) and a p38 MAPK inhibitor (SB203580). Inhibition of AMPK activity reduced p38 MAPK phosphorylation, whereas the inhibition of p38 MAPK activity did not affect AMPK phosphorylation. Pretreatment with the phosphatidylinositol 3-kinase inhibitor LY294002 and Compound C reduced PLE-stimulated glucose uptake. Our results demonstrate that PLE stimulated glucose uptake by activating both insulin signalling and AMPK-p38 MAPK pathways. PLE shows potential as a natural antihyperglycaemic agent.

摘要

樱花被用作一种药用植物来缓解糖尿病的症状;然而,其降血糖活性的分子机制尚不清楚。在这项研究中,我们研究了樱花的降血糖作用及其分子机制。樱花叶提取物(PLE)增加了胰岛素受体底物(IRS)-1、3'-磷酸肌醇依赖性激酶(PDK)-1和 Akt 的磷酸化,同时也增加了 AMP 激活的蛋白激酶(AMPK)和 p38 丝裂原活化蛋白激酶(p38 MAPK)的磷酸化。AMPK 抑制剂(Compound C)和 p38 MAPK 抑制剂(SB203580)阻断了 PLE 刺激的葡萄糖摄取。PLE 刺激的葡萄糖摄取被 AMPK 抑制剂(Compound C)和 p38 MAPK 抑制剂(SB203580)抑制。抑制 AMPK 活性降低了 p38 MAPK 的磷酸化,而抑制 p38 MAPK 活性并不影响 AMPK 的磷酸化。PI3K 抑制剂 LY294002 和 Compound C 的预处理降低了 PLE 刺激的葡萄糖摄取。我们的结果表明,PLE 通过激活胰岛素信号和 AMPK-p38 MAPK 途径来刺激葡萄糖摄取。PLE 有望成为一种天然的降血糖药物。

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