CAJ | 학술논문

目的观察刨伤性脑损伤(traumatic brain injury,TBI)大鼠脑组织匀浆及线粒体Na+-K+-ATP酶、Ca2+-ATP酶活性、神经细胞内游离Ca2+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10 g·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7 d.分别于TBI后24 h、72 h、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、Ca2+-ATP酶活性、神经细胞内游离Ca2+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、Ca2+-ATP酶活性均明显降低,于TBI后72 h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、Ca2+-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Ca2+浓度及脑组织CaM表达均有不同程度增高,于伤后24 h达高峰,持续至72 h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Ca2+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、Ca2+-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Ca2+浓度及脑组织CaM表达,减轻Ca2+超载所导致的继发性脑损伤有关.
목적 관찰포상성뇌손상(traumatic brain injury,TBI)대서뇌조직균장급선립체Na+-K+-ATP매、Ca2+-ATP매활성、신경세포내유리Ca2+농도급뇌조직개조단백(CaM)표체적동태변화,탐토뇌복합제뇌보호작용적분자생물학궤제.방법 건립대서TBI모형,분별설립가수술조、TBI조급중약치료조.중약치료조급여뇌복합제10 g·kg-1·d-1,가수술조급TBI조급여동등제량등삼염수,2차/d,련속7 d.분별우TBI후24 h、72 h、1주등3개시상점처사대서,동태정량분석각조대서뇌조직균장급선립체Na+-K+-ATP매、Ca2+-ATP매활성、신경세포내유리Ca2+농도급뇌조직CaM표체적변화.결과 TBI조각시상점대서뇌조직균장급선립체Na+-K+-ATP매、Ca2+-ATP매활성균명현강저,우TBI후72 h후축점회복,1주시잉명현저우가수술조.중약치료조대서뇌조직Na+-K+-ATP매、Ca2+-ATP매활성현저증가(P＜0.05);TBI조각시상대서뇌조직신경세포내유리Ca2+농도급뇌조직CaM표체균유불동정도증고,우상후24 h체고봉,지속지72 h잉고우가수술조.이중약치료조각시상대서신경세포내유리Ca2+농도급뇌조직CaM표체명현저우TBI조(P＜0.05).결론 뇌복합제적뇌보호작용가능여증가뇌조직Na+-K+-ATP매、Ca2+-ATP매적활성,종이감경TBI후뇌세포적능량대사장애,강저신경세포내유리Ca2+농도급뇌조직CaM표체,감경Ca2+초재소도치적계발성뇌손상유관.
Objective To dynamically observe the effect of compound decotion on changes of Na+-K+-ATPase,Ca2+-ATPase activity,intracellular free Ca2+ contents and CaM expression jn 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 comof normal saline,twice per day for seven days.Rats were sacrificed at 24 h,72 h and 1 week after injury to dynamically observe activities of Na+-K+-ATPase and Ca2+-ATPase in bomogenate and mitochondria of rat brain tissues,concentration of free Ca2+ in neurocytes and expression change of CaM in brain tissues.Results The activities of Na+-K+-ATP ageand Ca2+-ATPase in homogenates and mitochondria of brain tissues markedly decreased at different time point and increased gradually after 72 hours in TBI group but wag still lower than that of sham operation group at one week after injury.However,compound decotion could significantly enhance the activities of Na+-K+-ATPageand Ca2+-ATPage(P＜0.05).In TBI group,concentration of free Ca2+ 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 Ca2+ 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 Ca2+-ATPase to facilitate cellular metabolism and decreasing concentration of free Ca2+ in neurocytes and CaM expression in brain tissues to mitigate secondary brain injury induced by Ca2+ over load.