Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic β-Cell Dysfunction and Apoptosis.
Sesamin Ameliorates Advanced Glycation End Products-Induced Pancreatic β-Cell Dysfunction and Apoptosis.
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芝麻素可改善晚期糖基化终产物诱导的胰腺 β 细胞功能障碍和细胞凋亡
作者：
Kong X;Wang GD;Ma MZ;Deng RY;Guo LQ;Zhang JX;Yang JR;Su Q
晚期糖基化终产物（AGEs）是β-细胞的直接调节剂，已被证明通过增加细胞内活性氧（ROS）的产生导致胰岛素生成β-细胞功能障碍和凋亡。芝麻素已被证明具有抗氧化活性。本研究旨在探讨芝麻素是否通过其抗氧化性来保护衰老引起的β细胞损伤。观察芝麻素对C57BL/6J小鼠和MIN6细胞系的影响。在体内研究中，小鼠腹腔注射AGEs (120 mg/kg)，并口服芝麻素（160 mg/kg） 4周。进行腹腔内葡萄糖耐量和胰岛素释放试验。测定胰岛胰岛素含量、ROS生成及β细胞凋亡。在体外实验中，先用芝麻素（50 μM或100 μM）预处理MIN6细胞，再用AGEs （200 mg/L）处理24 h，检测胰岛素分泌、β细胞死亡、ROS生成以及NADPH氧化酶的表达和活性。芝麻素处理在体内和体外均能明显改善age诱导的β细胞功能障碍和凋亡。这些影响与ROS生成减少、p67phox和p22phox表达下调以及NADPH氧化酶活性降低有关。这些结果表明芝麻素通过抑制NADPH氧化酶介导的氧化应激来保护β-细胞免受AGEs引起的损伤。
Advanced glycation end products (AGEs), the direct modulators of β-cells, have been shown to cause insulin-producing β-cell dysfunction and apoptosis through increase of intracellular reactive oxygen species (ROS) production. Sesamin has been demonstrated to possess antioxidative activity. This study was designed to investigate whether sesamin protects against AGEs-evoked β-cell damage via its antioxidant property. The effects of sesamin were examined in C57BL/6J mice and MIN6 cell line. In in vivo studies, mice were intraperitoneally injected with AGEs (120 mg/kg) and orally treated with sesamin (160 mg/kg) for four weeks. Intraperitoneal glucose tolerance and insulin releasing tests were performed. Insulin content, ROS generation and β-cell apoptosis in pancreatic islets were also measured. In in vitro studies, MIN6 cells were pretreated with sesamin (50 or 100 μM) and then exposed to AGEs (200 mg/L) for 24 h. Insulin secretion, β-cell death, ROS production as well as expression and activity of NADPH oxidase were determined. Sesamin treatment obviously ameliorated AGE-induced β-cell dysfunction and apoptosis both in vivo and in vitro. These effects were associated with decreased ROS production, down-regulated expression of p67phox and p22phox, and reduced NADPH oxidase activity. These results suggest that sesamin protects β-cells from damage caused by AGEs through suppressing NADPH oxidase-mediated oxidative stress.
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影响因子：
7.7
作者：
Coughlan MT;Yap FY;Tong DC;Andrikopoulos S;Gasser A;Thallas-Bonke V;Webster DE;Miyazaki J;Kay TW;Slattery RM;Kaye DM;Drew BG;Kingwell BA;Fourlanos S;Groop PH;Harrison LC;Knip M;Forbes JM
通讯作者：
Forbes JM
影响因子：
6
作者：
Kiso, Y
通讯作者：
Kiso, Y
影响因子：
--
作者：
Palipoch S;Punsawad C;Koomhin P;Suwannalert P
通讯作者：
Suwannalert P
影响因子：
7.4
作者：
Lenzen, S;Drinkgern, J;Tiedge, M
通讯作者：
Tiedge, M
晚期糖基化终产物通过氧化应激诱导胰腺β细胞损伤
影响因子：
7.2
作者：
Lin, N.;Zhang, H.;Su, Q.
通讯作者：
Su, Q.