Expression of superoxide dismutase in hyperglycemic focal cerebral ischemia in the rat
Expression of superoxide dismutase in hyperglycemic focal cerebral ischemia in the rat
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DOI：
10.1016/j.neuint.2004.06.010
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发表时间：
2004-12-01
影响因子：
4.2
通讯作者：
Hazell, AS
中科院分区：
文献类型：
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作者：
Bémeur, C;Ste-Marie, L;Hazell, AS
本研究探讨了高血糖诱导大鼠局灶性脑缺血后各种超氧化物歧化酶（SOD）和一氧化氮合酶（NOS）早期表达的可能性。在急性高血糖和正常血糖条件下，永久性大脑中动脉闭塞3 h后检测MnSOD、CuZnSOD、nNOS和eNOS mRNA和蛋白的表达。与血糖正常的大鼠相比，2,3,5-三苯四唑氯（TTC）治疗在死后发现高血糖大鼠缺血后有明显的梗死风险。虽然MnSOD、CuZnSOD、nNOS和eNOS mRNA表达未见变化，但与正常血糖大鼠相比，高血糖大鼠缺血皮质的MnSOD和CuZnSOD蛋白表达增加。用NOS抑制剂l -硝基精氨酸甲酯（L-NAME）和7-硝基茚唑（7-NI）或超氧化物清除剂脱氢抗坏血酸（DHA）预处理高血糖大鼠，可显著减少TTC划定区域。高血糖诱导的MnSOD和CuZnSOD转录后水平上调表明，在一氧化氮产生增加的情况下，超氧化物产生增加可能在高血糖卒中后损伤风险增加中起主要作用。(C) 2004 Elsevier Ltd.版权所有。
This study investigated the possibility that hyperglycemia induces early expression of various superoxide dismutases (SOD) and nitric oxide synthases (NOS) following focal cerebral ischemia in the rat. MnSOD, CuZnSOD, nNOS and eNOS mRNA and protein expression were examined 3 h after permanent middle cerebral artery occlusion under acute hyperglycemic or normoglycemic conditions. 2,3,5-triphenyltetrazolium chloride (TTC) treatment post-mortem revealed a significant area at risk of infarction following ischemia in hyperglycemic compared to normoglycemic rats. Although no changes in MnSOD, CuZnSOD, nNOS and eNOS mRNA expression were detected, Western blots of ischemic cortex revealed an increase in MnSOD and CuZnSOD protein expression in hyperglycemic compared to normoglycemic rats. Pre-treatment of hyperglycemic rats with the NOS inhibitors L-nitroarginine methyl ester (L-NAME) and 7-nitroindazole (7-NI) or dehydroascorbic acid (DHA), a superoxide scavenger, significantly reduced the TTC delineated zone. The hyperglycemia-induced post-transcriptional upregulation of MnSOD and CuZnSOD levels suggest a response to increased superoxide production which, in the presence of increased nitric oxide production, may play a major role in the increased risk of damage following hyperglycemic stroke. (C) 2004 Elsevier Ltd. All rights reserved.