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茶籽皂苷还原提取物改善棕榈酸诱导的 HepG2 细胞胰岛素抵抗。

Tea seed saponin‑reduced extract ameliorates palmitic acid‑induced insulin resistance in HepG2 cells.

机构信息

Department of Chemistry, National Cheng Kung University, Tainan 701, Taiwan, R.O.C.

出版信息

Mol Med Rep. 2024 Feb;29(2). doi: 10.3892/mmr.2023.13149. Epub 2023 Dec 15.

Abstract

Tea () seed cake is a potential resource that contains a wealth of bioactive compounds. However, the high toxicity of tea saponins in tea seed cake restricts its applications. The present study aimed to i) develop a method of extracting bioactive compounds and reducing tea saponins during the process of tea seed cake extraction and ii) investigate the anti‑insulin resistance effect of tea seed saponin‑reduced extract (TSSRE) in a palmitic acid (PA)‑induced insulin resistance HepG2‑cell model. The concentration of tea saponins in TSSRE was ~10‑fold lower than that in tea seed crude extract (TSCE) after the saponin‑reduction process. In addition, TSSRE cytotoxicity was significantly lower than that of TSCE in HepG2 cells. TSSRE treatment improved glucose consumption as well as glucose transporter (GLUT) 2 and GLUT4 expression levels in PA‑stimulated HepG2 cells. Moreover, TSSRE enhanced the phosphorylation of the insulin receptor substrate 1/protein kinase B/forkhead box protein O1/glycogen synthase kinase 3β and inhibited the elevated expression of phosphoenolpyruvate carboxykinase in PA‑exposed HepG2 cells. The effect of TSSRE on the mediation of the insulin signaling pathway was attributed to the inhibition of PA‑induced mitogen‑activated protein kinase activation. The findings of the present study indicated that TSSRE ameliorates hepatic insulin resistance by ameliorating insulin signaling and inhibiting inflammation-related pathways.

摘要

茶籽饼是一种潜在的资源,含有丰富的生物活性化合物。然而,茶籽饼中茶皂素的高毒性限制了其应用。本研究旨在:i)开发一种在茶籽饼提取过程中提取生物活性化合物和降低茶皂素的方法;ii)研究茶皂素降低提取物(TSSRE)在棕榈酸(PA)诱导的胰岛素抵抗 HepG2 细胞模型中的抗胰岛素抵抗作用。经过脱皂素处理后,TSSRE 中的茶皂素浓度比茶籽粗提物(TSCE)中的茶皂素浓度低约 10 倍。此外,TSSRE 在 HepG2 细胞中的细胞毒性明显低于 TSCE。TSSRE 处理可改善 PA 刺激的 HepG2 细胞中的葡萄糖消耗以及葡萄糖转运蛋白(GLUT)2 和 GLUT4 的表达水平。此外,TSSRE 增强了胰岛素受体底物 1/蛋白激酶 B/叉头框蛋白 O1/糖原合酶激酶 3β的磷酸化,并抑制了 PA 暴露的 HepG2 细胞中磷酸烯醇丙酮酸羧激酶的升高表达。TSSRE 对胰岛素信号通路的调节作用归因于对 PA 诱导的丝裂原活化蛋白激酶激活的抑制作用。本研究结果表明,TSSRE 通过改善胰岛素信号和抑制炎症相关通路来改善肝胰岛素抵抗。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/27c2/10784731/8697727c7462/mmr-29-02-13149-g00.jpg

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