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黄芩苷对大鼠肌管中葡萄糖转运蛋白4(GLUT4)表达及葡萄糖摄取的影响

Effect of baicalin on GLUT4 expression and glucose uptake in myotubes of rats.

作者信息

Fang Penghua, Yu Mei, Min Wen, Wan Dan, Han Shiyu, Shan Yizhi, Wang Rui, Shi Mingyi, Zhang Zhenwen, Bo Ping

机构信息

Department of Physiology, Nanjing University of Chinese Medicine Hanlin College, Taizhou, Jiangsu 225300, China; Department of Endocrinology, Clinical Medical College, Yangzhou University, Yangzhou, Jiangsu 225001, China.

Department of Physiology, Nanjing University of Chinese Medicine Hanlin College, Taizhou, Jiangsu 225300, China.

出版信息

Life Sci. 2018 Mar 1;196:156-161. doi: 10.1016/j.lfs.2018.01.022. Epub 2018 Feb 2.

Abstract

AIMS

Although baicalin could attenuate obesity-induced insulin resistance, the detailed mechanism of baicalin on glucose uptake has not been sufficiently explored as yet. The aim of this study was to survey if baicalin might facilitate glucose uptake and to explore its signal mechanisms in L6 myotubes.

MATERIALS AND METHODS

L6 myotubes were treated with 100, 200, 400 μM baicalin for 6 h, 12 h and 24 h in this study. Then 2-NBDG and insulin signal protein levels in myotubes of L6 cells were examined.

KEY FINDINGS

We discovered that administration of baicalin enhanced GLUT4, PGC-1α, pP38MAPK, pAKT and pAS160 contents, as well as GLUT4 mRNA and PGC-1α mRNA levels in L6 myotubes. The beneficial metabolic changes elicited by baicalin were abrogated in myotubes of L6 by P38MAPK or AKT inhibitors.

SIGNIFICANCE

These results suggest that baicalin promoted glucose uptake in myotubes by differential regulation on P38MAPK and AKT activity. In conclusion, these data provide insight that baicalin is a powerful and promising agent for the treament of hyperglycemia via AKT/AS160/GLUT4 and P38MAPK/PGC1α/GLUT4 pathway.

摘要

目的

尽管黄芩苷可减轻肥胖诱导的胰岛素抵抗,但黄芩苷对葡萄糖摄取的详细机制尚未得到充分研究。本研究的目的是探讨黄芩苷是否能促进葡萄糖摄取,并在L6肌管中探索其信号机制。

材料与方法

本研究中,用100、200、400μM黄芩苷处理L6肌管6小时、12小时和24小时。然后检测L6细胞肌管中的2-NBDG和胰岛素信号蛋白水平。

主要发现

我们发现给予黄芩苷可提高L6肌管中GLUT4、PGC-1α、pP38MAPK、pAKT和pAS160的含量,以及GLUT4 mRNA和PGC-1α mRNA水平。P38MAPK或AKT抑制剂可消除黄芩苷在L6肌管中引起的有益代谢变化。

意义

这些结果表明,黄芩苷通过对P38MAPK和AKT活性的差异调节促进肌管中的葡萄糖摄取。总之,这些数据表明黄芩苷是一种通过AKT/AS160/GLUT4和P38MAPK/PGC1α/GLUT4途径治疗高血糖的有力且有前景的药物。

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