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乙酰紫草素通过 PLC-β3/PKCδ 依赖途径刺激 L6 肌管摄取葡萄糖。

Acetylshikonin stimulates glucose uptake in L6 myotubes via a PLC-β3/PKCδ-dependent pathway.

机构信息

Department of Pharmacology, Cardiac and Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China; Department of Pharmacy, Maoming People's Hospital, Maoming, China.

Department of Pharmacology, Cardiac and Cerebral Vascular Research Center, Zhongshan School of Medicine, Sun Yat-Sen University, Guangzhou, China.

出版信息

Biomed Pharmacother. 2019 Apr;112:108588. doi: 10.1016/j.biopha.2019.01.049. Epub 2019 Feb 16.

DOI:10.1016/j.biopha.2019.01.049
PMID:30780104
Abstract

Acetylshikonin, a naphthoquinone derivative derived from Lithospermum erythrorhizon, has been shown to have various pharmacological activities; however, its effect on diabetes has rarely been reported. We investigated the hypoglycemic effect of acetylshikonin and found that it decreased blood glucose to a greater extent than insulin and improved glucose tolerance in mice. It also increased glucose uptake in L6 myotubes by inducing the expression and translocation of glucose transporter 4 via decomposition of phosphatidylinositol, increased generation of diacylglycerol, and activation of protein kinase C delta cascades; this is an insulin-, reactive oxygen species-, and AMP-activated protein kinase-independent pathway for glucose uptake. Our findings highlight the antidiabetic potential of acetylshikonin via a possible novel pathway for glucose uptake in L6 myotubes.

摘要

乙酰紫草素是一种来源于紫草的萘醌衍生物,具有多种药理活性;然而,其对糖尿病的作用鲜有报道。我们研究了乙酰紫草素的降血糖作用,发现其降血糖作用强于胰岛素,并改善了小鼠的葡萄糖耐量。它还通过分解磷酸肌醇诱导葡萄糖转运蛋白 4 的表达和易位,增加 L6 肌管中的葡萄糖摄取,增加二酰基甘油的产生,并激活蛋白激酶 C 德尔塔级联,从而增加葡萄糖摄取;这是一种胰岛素、活性氧和 AMP 激活蛋白激酶非依赖性的葡萄糖摄取途径。我们的研究结果强调了乙酰紫草素通过一种可能的新型途径在 L6 肌管中摄取葡萄糖的抗糖尿病潜力。

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