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月桂酸通过激活GPR84和PI3K/Akt信号通路刺激青春期小鼠乳腺发育。

Lauric Acid Stimulates Mammary Gland Development of Pubertal Mice through Activation of GPR84 and PI3K/Akt Signaling Pathway.

作者信息

Meng Yingying, Zhang Jing, Zhang Fenglin, Ai Wei, Zhu Xiaotong, Shu Gang, Wang Lina, Gao Ping, Xi Qianyun, Zhang Yongliang, Liang Xingwei, Jiang Qingyan, Wang Songbo

机构信息

College of Animal Science and National Engineering Research Center for Breeding Swine Industry, South China Agricultural University , Guangzhou 510642, P. R. China.

ALLTECH-SCAU Animal Nutrition Control Research Alliance, South China Agricultural University , Guangzhou 510642, P. R. China.

出版信息

J Agric Food Chem. 2017 Jan 11;65(1):95-103. doi: 10.1021/acs.jafc.6b04878. Epub 2016 Dec 22.

DOI:10.1021/acs.jafc.6b04878
PMID:27978622
Abstract

It has been demonstrated that dietary fat affects pubertal mammary gland development. However, the role of lauric acid (LA) in this process remains unclear. Thus, this study aimed to investigate the effects of LA on mammary gland development in pubertal mice and to explore the underlying mechanism. In vitro, 100 μM LA significantly promoted proliferation of mouse mammary epithelial cell line HC11 by regulating expression of proliferative markers (cyclin D1/3, p21, PCNA). Meanwhile, LA activated the G protein-coupled receptor 84 (GPR84) and PI3K/Akt signaling pathway. In agreement, dietary 1% LA enhanced mammary duct development, increased the expression of GPR84 and cyclin D1, and activated PI3K/Akt in mammary gland of pubertal mice. Furthermore, knockdown of GPR84 or inhibition of PI3K/Akt totally abolished the promotion of HC11 proliferation induced by LA. These results showed that LA stimulated mammary gland development of pubertal mice through activation of GPR84 and PI3K/Akt signaling pathway.

摘要

已有研究表明,膳食脂肪会影响青春期乳腺发育。然而,月桂酸(LA)在此过程中的作用仍不清楚。因此,本研究旨在探讨LA对青春期小鼠乳腺发育的影响,并探究其潜在机制。在体外实验中,100μM的LA通过调节增殖标志物(细胞周期蛋白D1/3、p21、增殖细胞核抗原)的表达,显著促进了小鼠乳腺上皮细胞系HC11的增殖。同时,LA激活了G蛋白偶联受体84(GPR84)和PI3K/Akt信号通路。同样,在饮食中添加1%的LA可促进青春期小鼠乳腺导管发育,增加GPR84和细胞周期蛋白D1的表达,并激活乳腺中的PI3K/Akt。此外,敲低GPR84或抑制PI3K/Akt可完全消除LA诱导的HC11增殖促进作用。这些结果表明,LA通过激活GPR84和PI3K/Akt信号通路刺激青春期小鼠乳腺发育。

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