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肉桂单宁 D-1 通过减轻氧化应激来保护胰岛β细胞免受棕榈酸诱导的细胞凋亡。

Cinnamtannin D-1 protects pancreatic β-cells from palmitic acid-induced apoptosis by attenuating oxidative stress.

机构信息

Shanghai Institute of Materia Medica, Chinese Academy of Sciences , Shanghai 201203, China.

出版信息

J Agric Food Chem. 2014 Jun 4;62(22):5038-45. doi: 10.1021/jf500387d. Epub 2014 May 22.

Abstract

In previous studies, A-type procyanidin oligomers isolated from Cinnamomum tamala were proved to possess antidiabetic effect and protect pancreatic β-cells in vivo. The aim of this study was to unveil the mechanisms of protecting pancreatic β-cells from palmitic acid-induced apoptosis by cinnamtannin D-1 (CD1), one of the main A-type procyanidin oligomers in C. tamala. CD1 was discovered to dose-dependently reduce palmitic acid- or H2O2-induced apoptosis and oxidative stress in INS-1 cells, MIN6 cells, and primary cultured murine islets. Moreover, CD1 could reverse palmitic acid-induced dysfunction of glucose-stimulated insulin secretion in primary cultured islets. These results indicate that reduction of apoptosis and oxidative stress might account for the protection effect of CD1, which provided a better understanding of the mechanisms of the antidiabetic effects of procyanidin oligomers.

摘要

在先前的研究中,从肉桂中分离出的 A 型原花青素低聚物被证明具有抗糖尿病作用,并能在体内保护胰岛β细胞。本研究旨在揭示肉桂单宁 D-1(CD1)的作用机制,CD1 是肉桂中主要的 A 型原花青素低聚物之一,可防止棕榈酸诱导的胰岛β细胞凋亡。结果发现,CD1 可剂量依赖性地降低 INS-1 细胞、MIN6 细胞和原代培养的胰岛中棕榈酸或 H2O2 诱导的细胞凋亡和氧化应激。此外,CD1 还可以逆转棕榈酸诱导的原代培养胰岛中葡萄糖刺激的胰岛素分泌功能障碍。这些结果表明,凋亡和氧化应激的减少可能是 CD1 保护作用的原因,这为理解原花青素低聚物的抗糖尿病作用机制提供了更好的认识。

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