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人参皂苷 Rg3 抑制棕榈酸诱导的 MIN6N8 胰岛β细胞凋亡。

Ginsenoside Rg3 Suppresses Palmitate-Induced Apoptosis in MIN6N8 Pancreatic beta-Cells.

机构信息

Functional Food Technology Research Group, Research Division for Emerging Innovative Techology, Korea Food Research Institute, 516 Baekhyun-dong, Bundang-gu, Songnam-si, Kyonggi-do 463-746, Republic of Korea.

出版信息

J Clin Biochem Nutr. 2010 Jan;46(1):30-5. doi: 10.3164/jcbn.09-49. Epub 2009 Dec 29.

Abstract

Chronic exposure to elevated levels of free fatty acids (FFA) causes beta-cell dysfunction and may induce beta-cell apoptosis in type 2 diabetes. The execution of beta-cell apoptosis occurs through activation of mitogen-activated protein kinases (MAPKs). Ginsenoside Rg3 (Rg3), one of the active ingredients of ginseng saponins, has not been known about the effects on beta-cell apoptosis mediated with FFA. The aims of this study were to investigate the in vitro protective effects of Rg3 on MIN6N8 mouse insulinoma beta-cells against FFA-induced apoptosis, as well as the modulating effects on p44/42 MAPK activation. Our results showed that Rg3 inhibited the palmitate-induced apoptosis through modulating p44/42 MAPK activation. We conclude that Rg3 has the potential role in suppressing the progression of type 2 diabetes by inhibiting FFA-mediated loss of beta-cells.

摘要

慢性暴露于高水平的游离脂肪酸(FFA)可导致β细胞功能障碍,并可能在 2 型糖尿病中诱导β细胞凋亡。β细胞凋亡的执行是通过激活丝裂原活化蛋白激酶(MAPK)来实现的。人参皂苷 Rg3(Rg3)是人参皂苷的一种活性成分,目前还不清楚它对 FFA 介导的β细胞凋亡的影响。本研究旨在探讨 Rg3 对 MIN6N8 小鼠胰岛素瘤β细胞在体外抵抗 FFA 诱导的凋亡的保护作用,以及对 p44/42 MAPK 激活的调节作用。我们的结果表明,Rg3 通过调节 p44/42 MAPK 的激活来抑制软脂酸诱导的细胞凋亡。我们的结论是,Rg3 通过抑制 FFA 介导的β细胞丢失,有可能抑制 2 型糖尿病的进展。

https://cdn.ncbi.nlm.nih.gov/pmc/blobs/299e/2803130/f5170fc90abb/jcbn09-49f01.jpg

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