Methylglyoxal induces apoptosis through activation of p38 MAPK in rat Schwann cells
Methylglyoxal induces apoptosis through activation of p38 MAPK in rat Schwann cells
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DOI：
10.1016/j.bbrc.2004.06.011
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发表时间：
2004-07-30
影响因子：
3.1
通讯作者：
Kasuga, M
中科院分区：
文献类型：
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作者：
Fukunaga, M;Miyata, S;Kasuga, M
葡萄糖衍生的甲基乙二醛（MG）是一种高活性的二羰基化合物，在糖尿病条件下加速形成。我们研究了MG是否能够诱导雪旺细胞（SCs）凋亡，因为最近的研究表明，凋亡细胞死亡可能参与糖尿病神经病变的发展。MG以剂量依赖性的方式诱导SCs凋亡，同时伴随着细胞内谷胱甘肽含量的减少和p38 MAPK的激活。SB203580抑制p38 MAPK激活成功抑制mg诱导的sc细胞凋亡。氨基胍和n -乙酰- l-半胱氨酸也能抑制mg诱导的p38 MAPK激活和凋亡，同时恢复细胞内谷胱甘肽含量。这些结果表明，在糖尿病条件下，MG通过氧化应激介导的p38 MAPK激活在SC损伤中发挥潜在作用，并可能为糖尿病神经病变的治疗策略提供新的见解。(C) 2004爱思唯尔公司版权所有。
The formation of glucose-derived methylglyoxal (MG), a highly reactive dicarbonyl compound, is accelerated under diabetic conditions. We examined whether MG was capable of inducing apoptosis in Schwann cells (SCs), since recent studies have suggested a potential involvement of apoptotic cell death in the development of diabetic neuropathy. MG induced apoptosis in SCs in a dose-dependent manner, accompanied by a reduction of intracellular glutathione content and activation of the p38 MAPK. Inhibiting the p38 MAPK activation by SB203580 successfully suppressed the MG-induced apoptosis in SCs. Aminoguanidine and N-acetyl-L-cysteine also inhibited the MG-induced p38 MAPK activation and apoptosis along with restoration of the intracellular glutathione content. These results suggest a potential role for MG in SC injury through oxidative stress-mediated p38 MAPK activation under diabetic conditions, and it may serve as a novel insight into therapeutic strategies for diabetic neuropathy. (C) 2004 Elsevier Inc. All rights reserved.