长期慢性脑外伤大鼠脑线粒体功能的变化

Changes of Cortex Mitochondrial Function in Chronic Traumatic Brain Injury Rats

研究长期慢性轻度脑外伤对大鼠脑线粒体功能的影响。大鼠连续1、5、10、15、20、25、30d轻度闭合性颅脑撞击后分离脑线粒体,测定线粒体肿胀度、膜流动性、膜磷脂含量、呼吸功能、线粒体呼吸酶、超氧化物歧化酶(SOD)、丙二醛(MDA)和Ca2+等指标以显示线粒体功能、抗氧化能力的变化。结果显示,第15、20、25、30d大鼠脑线粒体明显肿胀,膜磷脂降解,膜流动性下降,呼吸功能衰减,呼吸酶、SOD活性降低,Ca2+、MDA含量升高。由此认为,经常性头部撞击可造成大鼠脑线粒体功能受损,其机制可能与脑线粒体膜损伤后继发的自由基生成增加、脑线粒体能量代谢障碍有关。

This experimental study was aimed to evaluate the injurious effects of chronic traumatic brain injury on cortex mitochondrial function in rats. The head of rat was impacted by a metal sphere in a weight-drop device twice per day for 30 days, cortex mitochondria were isolated. Then the mitochondria membrane fluidity, swelling, respiratory function, the activities of mitochondria respiratory enzymes and superoxide dismutase （SOD）, the levels of phospholipid, malondial dehyde （MDA） and Ca^2＋ were determined to analyze the function of mitochondria. The data indicated that chronic closed traumatic brain injury caused severe neuronal mitochondrial injuries. The swelling of mitochondria was aggravated, the decomposability of mitochondrial membrane phospholipid was increased, the membrane fluidity of mitochondria was decreased;the chronic closed traumatic brain injury also significantly depressed the activities of respiratory enzymes and SOD of mitochondria, increased the level of MDA and Ca^2＋. The chronic closed traumatic brain injury induced damage to rat cortex mitochondria. The mechanisms may be derived from the secondary increase of free radicals induced by mitochondrial membrane injury and the obstacle of rat brain energy metabolism.