Effect of compound decotion on activities of Na+-K+-ATPase and Ca2+-ATPase and regulation of Ca2+ after traumatic brain injury / 中华创伤杂志

ABSTRACT

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.