Effect of hypothermia on expression of dynamin-related protein 1 in brain tissues during global cere-bral ischemia-reperfusion in rats / 中华麻醉学杂志

ABSTRACT

Objective To evaluate the effect of hypothermia on the expression of dynamin?related protein 1 ( Drp1) in brain tissues during global cerebral ischemia?reperfusion ( I∕R) in rats. Methods Thirty?six healthy male Sprague?Dawley rats, weighing 280-320 g, were divided into 3 groups ( n=12 each) using a random number table sham operation group ( group Sham ) , global cerebral I∕R group ( group I∕R) and hypothermia group ( group H) . Cardiac arrest was induced by transoesophageal cardiac pacing followed by cardiopulmonary resuscitation to establish the global cerebral I∕R model in anesthetized rats in I∕R and H groups. In group H, the body temperature ( rectal temperature) was cooled down to 32-34 ℃ within 15 min starting from the beginning of reperfusion, and maintained at this level for 6 h. At 72 h of reperfusion, neurological deficit was scored, and the rats were sacrificed, and the whole brain was removed for examination of the pathological changes in hippocampal CA1 region and for determination of nor?mal pyramidal cell count and neuronal apoptosis in hippocampal CA1 region and expression of Drp1 and cy?tochrome c (Cyt c) in hippocampal tissues (by Western blot). The apoptosis rate was calculated. Re?sults Compared with group S, the neurological deficit score and apoptosis rate were significantly in?creased, and the number of normal pyramidal cells was decreased in I∕R and H groups, the expression of Drp1 and Cyt c in hippocampal tissues was significantly up?regulated in group I∕R ( P0.05) . Compared with group I∕R, the neurological deficit score and apoptosis rate were significantly de?creased, the number of normal pyramidal cells was increased, and the expression of Drp1 and Cyt c in hip?pocampal tissues was down?regulated in group H ( P<0.05) . Conclusion The mechanism by which hypo?thermia inhibits cell apoptosis during global cerebral I∕R may be related to down?regulation of Drp1 expres?sion in rats.