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叔丁基对苯二酚预处理对大鼠创伤性脑损伤的保护作用研究 被引量：8

Protective effect of t-BHQ pretreatment on traumatic brain injury in rats
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摘要 目的氧化应激是创伤性颅脑损伤后重要继发性病理生理反应,新近研究发现,Nrf2-ARE信号路径具有抗氧化作用。文中拟验证Nrf2诱导剂叔丁基对苯二酚(tertiary buty lhydroquinone,t-BHQ)预处理对创伤性脑损伤后大鼠的脑保护作用。方法将54只SD大鼠随机分为对照组、损伤组和给药组,每组18只。给药组大鼠颅脑创伤前24h腹腔预注射t-BHQ,采用改良的Feeney′s自由落体方法制作颅脑外伤模型,伤后24h应用干湿重比方法测定各组大鼠局部损伤脑组织含水量、应用原位末端标记法(terminal deoxynudeotidyl transferase mediated duTP nick end labeling assay,TUNEL)检测细胞凋亡。结果t-BHQ可降低大鼠脑损伤后脑皮质含水量,病理学检查结果也证实,t-BHQ预处理可显著减轻损伤神经元的凋亡指数。结论t-BHQ预处理可有效地保护创伤性脑损伤后大鼠损伤脑组织。 Objective Oxidative stress is a key pathophysiological response to traumatic brain injury （TBI）. The Nrf2-ARE signal pathway has been found to have an antioxidative effect. This study aimed to verify the protective effect of Nrf2 inducer t-BHQ on traumatic brain injury in rats. Methods Fifty-four SD rats were equally randomized to three groups： control, TBI and medication. The rats in the medication group were intraperitoneally injected with t-BHQ 24 hours before brain trauma, and TBI was induced by Feeney＇s free weight drop method. Water content of the local brain tissue was measured, and apoptotic cells were detected by TUNEL 24 hours after brain trauma. Results Pretreatment with t-BHQ significantly decreased the local content of water and the apoptosis of the injured neurons. Conclusion Pretreatment with t-BHQ can effectively protect the damaged brain tissues after traumatic brain injury.
作者 宋亚颀 王汉东 闫伟 乔梁 王庆丰 金伟 印红霞
机构地区 南京大学医学院临床学院(南京军区南京总医院)神经外科 淮安市第一人民医院放疗科
出处 《医学研究生学报》 CAS 2010年第4期365-368,共4页 Journal of Medical Postgraduates
基金 江苏省医学重点学科基金(X4200722) 南京军区重点课题(07Z029)
关键词 创伤性脑损伤 脑水肿 凋亡 叔丁基对苯二酚 Traumatic brain injury Brain edema Apoptosis Tertiary butylhydroquinone
分类号 R742.7 [医药卫生—神经病学与精神病学]
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参考文献16

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共引文献29

同被引文献58

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医学研究生学报
2010年 第4期

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