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葡萄糖对四氧嘧啶诱导的胰腺β细胞损伤的保护机制。

Protective mechanism of glucose against alloxan-induced pancreatic beta-cell damage.

作者信息

Park B H, Rho H W, Park J W, Cho C G, Kim J S, Chung H T, Kim H R

机构信息

Department of Biochemistry, Chonbuk National University Medical School, Chonju, Republic of Korea.

出版信息

Biochem Biophys Res Commun. 1995 May 5;210(1):1-6. doi: 10.1006/bbrc.1995.1619.

Abstract

Glucose prevented the alloxan- or H2O2-induced inhibition of insulin secretion in rat pancreatic islets. Hydrogen peroxide was detected during the incubation of islets with alloxan, and this generation of hydrogen peroxide was not affected by glucose. Treatment of beta-cells with alloxan or H2O2 caused elevation of cytosolic free Ca2+ and decrease of cellular NAD+. Glucose blocked the decrease of cellular NAD+ level, but did not abolish the increase of cytosolic Ca2+. These results indicate that glucose protected pancreatic beta-cell damage after the H2O2 generation and Ca2+ influx on a chain of reactions in the diabetogenesis of alloxan.

摘要

葡萄糖可防止四氧嘧啶或过氧化氢诱导的大鼠胰岛胰岛素分泌抑制。在用四氧嘧啶孵育胰岛的过程中检测到了过氧化氢,且过氧化氢的产生不受葡萄糖的影响。用四氧嘧啶或过氧化氢处理β细胞会导致胞质游离Ca2+升高和细胞内NAD+降低。葡萄糖可阻止细胞内NAD+水平的降低,但不能消除胞质Ca2+的升高。这些结果表明,在四氧嘧啶致糖尿病过程中,葡萄糖在过氧化氢生成和Ca2+内流引发的一系列反应后,对胰腺β细胞损伤具有保护作用。

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