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作 者:张霞婧[1] 何二涛[1] 贾济[1] 朱萧玲[1] 王强[1] 朱正华[1] 胡胜[1] 陈绍洋[1]
机构地区:[1]第四军医大学附属西京医院麻醉科,西安710032
出 处:《国际麻醉学与复苏杂志》2012年第4期246-250,共5页International Journal of Anesthesiology and Resuscitation
基 金:国家自然科学基金(81028006、81050032)
摘 要:目的观察氨磷汀对谷氨酸(glutamate,Gin)所致N9小胶质细胞损伤的保护作用。方法建立Glu损伤模型,探索最适氨磷汀浓度,实验分4组:空白对照组(Con组),正常培养小胶质细胞24h;Glu损伤组(Glu组),含10mmol/LG1u的培养基处理N9细胞24h;氨磷汀组(Ami+Glu组),含1mmol/L氨磷汀和10mmol/LGlu的培养基处理N9细胞24h;TBOA组(Ami+TBOA+Glu组),含100μmol/LTBOA、1mmol/L氨磷汀和10mmol/LGlu的培养液培养N9小胶质细胞24h。采用四甲基偶氮唑盐(MTT)法检测细胞代谢率,检测培养液乳酸脱氢酶(1actatedehydrogenase,LDH)、超氧化物歧化酶(superoxidedismutase,SOD)、一氧化氮(nitrogenmonoxide,NO)的含量,收集贴壁细胞超声破碎,检测谷胱甘肽(glutathione,GSH)含量。结果与损伤组比较,1mmol/L氨磷汀保护组细胞代谢率(88.9±1.7)%升高(P〈0.05),LDH释放量(141±40)%减少(P〈0.05)。SOD含量(128±13)%增加(P〈0.01),GSH含量(88±8)%增2I(P〈0.01),NO释放量(147±34)%下降(P〈0.01);该作用可被兴奋性氨基酸转运体(excitatoryaminoacidtransporter,EAAT)拮抗剂TBOA逆转。结论氨磷汀通过抗氧化机制减轻Glu对N9小胶质细胞的损伤。Objective To investigate the effects of Amifostine on glutamate (Glu) induced microglia injury. Methods There are 4 groups: Con group, N9 microgial was cultured normally for 24 h, Glu group, N9 microgial was treated with 10 mmol/L Glu, Ami±Glu group, N9 microgial was treated with 1 mmol/L Amifostine and 10 mmol/L Glu, Ami±TBOA±Glu group, N9 microgial was treated with 100μmol/L TBOA, 1 mmol/L Amifostine and 10 mmol/L Glu for 24 h. Metabolism of microglial, lactate dehydrogenase (LDH) release, superoxide dismutase (SOD) activity, nitrogen monoxide (NO) release and glutathione (GSH) level were evaluated. Results As compared to control group, microglial metabolism (88.9±1.7)% increased (P〈0.05), SOD activity (128±13)% increased (P〈0.01) and GSH level(88±8)% increased(P〈0.01), while LDH(141±40)% and NO(147~34)% release were decreased in Amifostine group. The effects of Amifostine could be reversed by the antagonist of excitatory amino acid transporters(EAAT) TBOA. Conclusions Amifostine protects N9 microglial Glu injury through its antioxidantive effects.
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