摘要
目的观察创伤『生脑损伤（traumatic brain injury，TBI）大鼠脑组织匀浆及线粒体Na^＋-K^＋-ATP酶、Ca^2＋-ATP酶活性、神经细胞内游离ca“浓度及脑组织钙调蛋白（CaM）表达的动态变化，探讨脑复合剂脑保护作用的分子生物学机制。方法建立大鼠TBI模型，分别设立假手术组、TBI组及中药治疗组。中药治疗组给予脑复合剂10g·kg^-1·d^-1，假手术组及TBI组给予同等剂量等渗盐水，2次／d，连续7d。分别于TBI后24h、72h、1周等3个时相点处死大鼠，动态定量分析各组大鼠脑组织匀浆及线粒体Na^＋-K^＋-ATP酶、Ca^2＋-ATP酶活性、神经细胞内游离Ca^2＋浓度及脑组织CaM表达的变化。结果TBI组各时相点大鼠脑组织匀浆及线粒体Na^＋-K^＋-ATP酶、Ca^2＋-ATP酶活性均明显降低，于TBI后72h后逐渐恢复，1周时仍明显低于假手术组．中药治疗组大鼠脑组织Na^＋-K^＋-ATP酶、Ca^2＋-ATP酶活性显著增加（P〈0．05）；TBI组各时相大鼠脑组织神经细胞内游离Ca^2＋浓度及脑组织CaM表达均有不同程度增高，于伤后24h达高峰，持续至72h仍高于假手术组。而中药治疗组各时相大鼠神经细胞内游离Ca^2＋浓度及脑组织CaM表达明显低于TBI组（P〈0．05）。结论脑复合剂的脑保护作用可能与增加脑组织Na^＋-K^＋-ATP酶、Ca^2＋-ATP酶的活性，从而减轻TBI后脑细胞的能量代谢障碍，降低神经细胞内游离Ca^2＋浓度及脑组织CaM表达，减轻Ca^2＋超载所导致的继发性脑损伤有关。
Objective To dynamically observe the effect of compound decotion on changes of Na^＋ -K^＋ -ATPase, Ca^2＋ -ATPase activity, intracellular free Ca^2＋ contents and CaM expression in bomogenate and mitochondria of rat brain tissues after traumatic brain injury （TBI） and investigate the molecular mechanism of neuroprotective effect of compound decotion. Methods Rat TBI models were made and divided into sham operation group, TBI group and compound decotion treatment group （treated with eompound decotion at 10 g·kg^-1·d^-1 ）. Sham operation group and TBI group were treated with same dose of normal saline, twice per day for seven days. Rats were sacrificed at 924- h, 72 h and 1 week after injury to dynamically observe activities of Na^＋-K^＋ -ATP ase and Ca^2＋ -ATPase in bomogenate and mitochondria of rat brain tissues, concentration of free Ca^2 ＋ in neurocytes and expression change of CaM in brain tissues. Results The activities of Na＋ -K~ -ATP aseand Ca^2＋ -ATPase in homogenates and mitochondria of brain tissues markedly decreased at different time point and increased gradually after 72 hours in TBI group but was still lower than that of sham operation group at one week after injury. However, compound decotion could significantly enhance the activities of Na＋ -K~ -ATP aseand Ca^2＋ -ATPase （ P 〈 0.05 ）. In TBI group, concentration of free Ca^2＋ in neurocytes and CaM expression in brain tissues were elevated at different degrees at different time point and reached peak at 24 hours after injury but still lower than that of sham operation group at 72 hours. While concentration of free Ca^2＋ in neurocytes and CaM expression in brain tissues were significantly lower than those of TBI group at different time point （P 〈 0.05）. Conclusions The neuroprotective effect of compound decotion may be related to its role in increasing activities of Na＋ -K~ -ATPase and Ca^2＋ -ATPase to facilitate cellular metabolism and decreasing concentration of free Ca^2＋ in neurocytes and CaM ex
出处
《中华创伤杂志》
CAS
CSCD
北大核心
2008年第12期1002-1006,共5页
Chinese Journal of Trauma
基金
重庆市卫生局中医药科研资助项目（渝中医20024270）
关键词
脑损伤
三磷酸腺苷酶
钙调蛋白
Brain injuries
Adenosinetriphosphatase
Calmodulin
