Suppr超能文献

多糖通过恢复线粒体功能和调节 MAPK 和 AMPK/Akt/mTOR 信号通路预防棕榈酸诱导的肠上皮细胞凋亡和自噬。

Polysaccharides Prevent Palmitic Acid-Evoked Apoptosis and Autophagy in Intestinal Porcine Epithelial Cell Line via Restoration of Mitochondrial Function and Regulation of MAPK and AMPK/Akt/mTOR Signaling Pathway.

机构信息

Hunan Agricultural Product Processing Institute, Hunan Academy of Agricultural Sciences, Changsha 410125, China.

College of Veterinary Medicine, Hunan Agricultural University, Changsha 410128, China.

出版信息

Int J Mol Sci. 2019 Jan 23;20(3):478. doi: 10.3390/ijms20030478.

Abstract

polysaccharide (GLP) extracted from (Leyss. ex Fr.) Karst, a traditional Chinese medicine, is a biologically active substance reported to possess anti-oxidative, anti-apoptotic, and neurological protection. However, it is unknown whether GLP have any protective effect against high-fat constituents-induced epithelial cell injury. The aim of this study was to investigate the protection and molecular mechanism of GLP on injury induced by palmitic acid (PA) in the intestinal porcine epithelial cell line (IPEC-J2). First, we tested whether the treatment of GLP attenuate PA-induced IPEC-J2 cell death. GLP markedly blocked PA-caused cytotoxicity and apoptosis in IPEC-J2 cells. Moreover, GLP recovered the decreased mitochondrial function and inhibited activation of caspase-dependent apoptotic pathway. Interestingly, PA promoted cell apoptosis and autophagy through stimulation of phosphorylation of mitogen-activated protein kinases (MAPKs), AMP-activated protein kinase (AMPK), and inhibition of phosphorylation of Akt and mammalian target of rapamycin (mTOR), which was reversed by GLP. Taken together, this study revealed a protective effect of GLP against PA-evoked IPEC-J2 cell death through anti-apoptotic and anti-autophagic properties.

摘要

从(Leyss. ex Fr.)Karst 中提取的多糖(GLP)是一种具有生物活性的物质,据报道具有抗氧化、抗凋亡和神经保护作用。然而,目前尚不清楚 GLP 是否对高脂肪成分诱导的上皮细胞损伤有任何保护作用。本研究旨在探讨 GLP 对猪肠上皮细胞系(IPEC-J2)中棕榈酸(PA)诱导的损伤的保护作用及其分子机制。首先,我们检测了 GLP 是否能减轻 PA 诱导的 IPEC-J2 细胞死亡。GLP 显著抑制了 PA 引起的 IPEC-J2 细胞毒性和凋亡。此外,GLP 恢复了因 PA 引起的线粒体功能下降,并抑制了 caspase 依赖性凋亡途径的激活。有趣的是,PA 通过刺激丝裂原活化蛋白激酶(MAPKs)、AMP 激活蛋白激酶(AMPK)的磷酸化和抑制 Akt 和雷帕霉素靶蛋白(mTOR)的磷酸化来促进细胞凋亡和自噬,而 GLP 则逆转了这一过程。综上所述,本研究揭示了 GLP 通过抗凋亡和抗自噬特性对 PA 诱导的 IPEC-J2 细胞死亡的保护作用。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/547c/6387170/a46a4268dcdd/ijms-20-00478-g001.jpg

文献检索

告别复杂PubMed语法,用中文像聊天一样搜索,搜遍4000万医学文献。AI智能推荐,让科研检索更轻松。

立即免费搜索

文件翻译

保留排版,准确专业,支持PDF/Word/PPT等文件格式,支持 12+语言互译。

免费翻译文档

深度研究

AI帮你快速写综述,25分钟生成高质量综述,智能提取关键信息,辅助科研写作。

立即免费体验