葡萄糖诱导产生硫化氢可能保护胰岛β细胞免受高糖诱导的凋亡性细胞死亡。
Glucose-induced production of hydrogen sulfide may protect the pancreatic beta-cells from apoptotic cell death by high glucose.
作者信息
Kaneko Yukiko, Kimura Toshihide, Taniguchi Shigeki, Souma Midori, Kojima Yumiko, Kimura Yuka, Kimura Hideo, Niki Ichiro
机构信息
Department of Pharmacology, Oita University Faculty of Medicine, 1-1 Idaigaoka, Hasama, Oita 879-5593, Japan.
出版信息
FEBS Lett. 2009 Jan 22;583(2):377-82. doi: 10.1016/j.febslet.2008.12.026. Epub 2008 Dec 25.
We examined the expression of the major H(2)S-producing enzymes, cystathionine-beta-synthase (CBS) and cystathionine-gamma-lyase (CSE). CBS was ubiquitously distributed in the mouse pancreas, but CSE was found only in the exocrine. Freshly isolated islets expressed CBS, while CSE was faint. However, high glucose increased the CSE expression in the beta-cells. L-Cysteine or NaHS suppressed islet cell apoptosis with high glucose, and increased glutathione content in MIN6 beta-cells. Pretreatment with L-cysteine improved the secretory responsiveness following stimulation with glucose. The CSE inhibitor DL-propargylglycine antagonized these L-cysteine effects. We suggest H(2)S may function as an 'intrinsic brake' which protects beta-cells from glucotoxicity.
我们检测了主要的产H₂S酶，胱硫醚-β-合酶（CBS）和胱硫醚-γ-裂解酶（CSE）的表达。CBS在小鼠胰腺中广泛分布，但CSE仅在外分泌腺中被发现。新鲜分离的胰岛表达CBS，而CSE表达较弱。然而，高糖可增加β细胞中CSE的表达。L-半胱氨酸或NaHS可抑制高糖条件下的胰岛细胞凋亡，并增加MIN6 β细胞中的谷胱甘肽含量。L-半胱氨酸预处理可改善葡萄糖刺激后的分泌反应性。CSE抑制剂DL-炔丙基甘氨酸可拮抗这些L-半胱氨酸的作用。我们认为H₂S可能作为一种“内在制动器”，保护β细胞免受糖毒性。
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