亚低温对创伤性脑损伤后线粒体α-酮戊二酸脱氢酶活性的影响  

Effect of mild hypothermia on the activities of α-ketoglutarate dehydrogenase of mitochondria following traumatic brain injury

作　　者：陆兆丰[1] 贾锋[1] 邱永明[1] 罗其中[1] 江基尧[1] 

机构地区：[1]上海交通大学医学院附属仁济医院神经外科,200127

出　　处：《中华神经外科杂志》2006年第11期659-662,共4页Chinese Journal of Neurosurgery

基　　金：国家重点基础研究项目(973;2005CB522600)

摘　　要：目的研究亚低温对脑损伤后病理学,α-酮戊二酸脱氢酶(α-ketoglutarate dehydrogenase complex,α-KGDHC)活性以及Caspase-3活性的影响。方法雄性SD大鼠50只随机分七组：假手术组(n=5),液压脑损伤常温组(1．8～2．2atm)(n=25),液压脑损伤亚低温组(n=20)。常温组伤后6h,24h,72h,7d检测创伤侧皮层、海马及丘脑线粒体α-KGDHC活性及Caspase-3的活性。伤后15min应用亚低温,30min内脑温降至33℃并维持4h,检测24h及72h酶活性以及Caspase-3的活性。以及亚低温对损伤后24h皮层丘脑及海马CA3区神经病理的影响。结果Fluoro-jade染色显示亚低温显著减少损伤后24h坏死神经元数目(P＜0．05),伤后24h及72h KGDHC酶的活性显著增加(P＜0．05)。伤后24h Caspase-3的活性显著降低(45%)。结论创伤性脑损伤后早期亚低温能够恢复能量代谢酶的活性,抑制神经元凋亡,减轻损伤后神经元的变性。Objective We investigated the activities of rate-limiting enzyme-KGDHC and Caspase-3 in brain after TBI. Methods Male Sprague-Dawley rats 50, randomly divided into seven groups： shamoperation（ n = 4） , moderate fluid-percussion TBI-C （ n = 20 ） , moderate fluid-percussion TBI-H （ n = 20 ）. After 6h to 7 days of survival, animals were killed, brain samples （ cerebral cortex, hippocampus and thalamus） were harvested for KGDHC and Caspase-3 activities assay. Fluoro-jade staining was used to evaluate the pathology. Results α-KGDHC activity significant decreased in injured cortex, hippocampus, and thalamus at each time point after TBI （ 15% - 47% ）. Caspase-3 activity significantly increased in injured cortex hippocampus, and thalamus at each time point after TBI. Early hypothermia significantly increased α-KGDHC activity and decreased Caspase-3 activity. At the same time attaneuated neuronal degeneration in ipsilateral cortex after TBI. Conclusion Early hypothermia could recover α-KGDHC.

关 键 词：创伤性脑损伤 α-酮戊二酸脱氢酶 亚低温 细胞凋亡 大鼠 

分 类 号：R651.15[医药卫生—外科学]