腺苷预处理对局灶性脑缺血再灌注损伤大鼠脑组织中内源性神经干细胞增殖的影响

Effect of adenosine pretreatment on endogenous neural stem cell proliferation in brain tissue of rats with focal cerebral ischemia-reperfusion injury

目的:探讨腺苷预处理对局灶性脑缺血再灌注损伤大鼠脑组织中内源性神经干细胞增殖的影响。方法:36只成年雄性SD大鼠随机分为假手术组、模型组和腺苷预处理组,每组12只。用线栓法制备大鼠大脑中动脉缺血再灌注模型。腺苷预处理组大鼠于术前连续3 d腹腔注射腺苷(1.5 mg/kg),假手术组和模型组大鼠腹腔注射等体积生理盐水。再灌7 d后,各组大鼠进行神经功能缺损评分,并检测脑组织中Nestin和Wnt1蛋白的表达。结果:假手术组大鼠均无神经功能缺损症状,模型组和腺苷预处理组大鼠神经功能缺损评分、脑组织中Nestin阳性细胞百分率和海马区脑组织中Wnt1蛋白表达高于假手术组(F=127.010、577.971和4 831.900,P<0.001);腺苷预处理组大鼠神经功能缺损评分低于模型组(P<0.05),大鼠脑组织中Nestin阳性细胞百分率、海马区脑组织中Wnt1蛋白表达高于模型组(P<0.05)。结论:腺苷可能通过上调Wnt1蛋白的表达促进内源性神经干细胞的增殖,从而有效改善再灌注损伤引起的神经功能缺损症状。

Aim：To investigate the effect of adenosine pretreatment on endogenous neural stem cell proliferation in brain tissue of rats with focal cerebral ischemia-reperfusion injury. MethodS：Thirty-six adult male SD rats were randomly divided into sham operation group,model group and adenosine pretreatment group,twelve in each group. Rat model of middle cerebral artery occlusion was established by suture-occluded method. Rats in adenosine pretreatment group were treated with adenosine（ 1.5 mg/kg） by intraperitoneal injection for 3 days before operation. The rats in sham operation group and model group were treated with the same volume of normal saline by intraperitoneal injection at the same time. Neurological function defect score were estimated in rats of each group. The Nestin positive cells and the expression of Wntl protein in brain tissue were observed. Results：The rats in sham operation group had no neurological function defect symptom. The neurological function defect score,Nestin positive cells in brain tissue,and the expression of Wntl protein in hippocampal tissue in model group and adenosine pretreatment group were significantly higher than those in sham operation group （ F = 127. 010,577. 971,4 831. 900;P 〈 0. 001 ）. Conclusion ： Adenosine can promote the neural stem cell proliferation by upregulating the expression of Wntl protein,which can effectively improve the neurological function defect symptom caused by reperfusion injury.