摘要
目的:观察亚低温对急性颅脑创伤(TBI)大鼠脑组织线粒体呼吸链酶活性的影响。方法:将24只雄性SD大鼠随机分为对照组、常温TBI组和亚低温TBI组,制作中度脑创伤模型。亚低温组伤后给予6h亚低温治疗(31℃～33℃)后复温,实验动物于伤后24h处死,取出左侧受伤大脑,采用密度梯度离心法提取线粒体,JanusgreenB染色光镜下观察线粒体活性,电镜鉴定其纯度,生化方法测定线粒体琥珀酸脱氢酶(SDH)、细胞色素C氧化酶(CCO)以及还原型烟酰胺二核苷酸(NADH)活性。结果:与对照组比较,常温TBI组线粒体呼吸链酶活性均下降(P<0.05);亚低温TBI组SDH活性(16.09±5.58)保持正常;与亚低温TBI组比较,常温TBI组SDH酶活性(3.46±1.82)降低(P<0.05),而CCO和NADH酶活性没有显著变化。结论:颅脑创伤后线粒体功能受损,酶活性有所下降,伤后亚低温治疗有助于维持线粒体琥珀酸脱氢酶活性,减少继发能量损失,保护脑组织。
Objective： To observe the effect of mild hypothermia treatment on respiratory chain enzymes of mitochondrion following traumatic brain injury （TBI）. Methods： Male Sprague-Dawley rats 24,randomly divided into three groups, normal control group （C,n = 8）,hypothermic injury group （HI,31 ℃-33 ℃ ,6 h,n = 8） and normothermic injury group （NI,36 ℃-37 ℃ ,n = 8）.The groups of HI and NI were subjected to moderate injury of left brain by lateral fluid pressure device. The ipsilateral brain samples were dissected and homogenized after 24 h TBI. Mitochondrion was extracted by density and speed-centrifugation. The activity and purity of mitochondrion were identified by Janus green B staining and electron microscopy（EM）respectively, and then activities of succinate dehydrogenase （SDH）, cytochrome C oxidase （CCO） and nicotinamide ade-nine dinucleotide （NADH） were tested. Results： Compared with C group, activities of CCO and NADH significantly decreased in NI group （P 〈 0.05 ）. Activity of SDH kept normal after 6 h TBI in HI group （P 〈 0.05）. Conclusion： These findings suggested that activity of mitochondrial respiratory chain enzymes decreased after TBI, and mild hypothermia could maintain the SDH activity of the mitochondrial after TBI and lighten the secondary energy loss, and then protect the brain tissue.
出处
《天津医药》
CAS
北大核心
2008年第7期524-526,共3页
Tianjin Medical Journal
基金
国家“973”计划子课题(项目编号:2005CB522604)
天津市“211”“重中之重”学科建设专项基金资助项目(项目编号:05YFGDSF02500)
