CAJ | 학술논문

目的研究皮层δ-阿片受体(δ-opioid receptor,DOR)的抗神经元氧糖剥夺损伤作用.方法采用原代培养胎鼠皮层神经元氧糖剥夺(oxygen-glucose deprivation,OGD)模型,分别加入DOR选择性激动剂TAN一67、拮抗剂nahrindole及PKC抑制剂chelerythrine(CHE),检测再灌注后培液中LDH水平、进行死/活细胞染色,并利用Western blot检测再灌注24 h后DOR蛋白表达水平.结果与单纯OGD组相比,OGD+TAN-67组培液中的LDH水平明显下降,荧光染色显示活细胞增加死细胞减少,且DOR蛋白表达增加;OGD+naltrindole组则细胞受损加重.且DOR蛋白表达减少.PKC抑制剂CHE能抑制DOR激活后培液中LDH水平的下调.结论 DOR激动剂可以抗神经元氧糖剥夺损伤.拮抗DOR则加重该损伤.PKC可能参与了DOR的神经保护作用.
목적 연구피층δ-아편수체(δ-opioid receptor,DOR)적항신경원양당박탈손상작용.방법 채용원대배양태서피층신경원양당박탈(oxygen-glucose deprivation,OGD)모형,분별가입DOR선택성격동제TAN일67、길항제nahrindole급PKC억제제chelerythrine(CHE),검측재관주후배액중LDH수평、진행사/활세포염색,병이용Western blot검측재관주24 h후DOR단백표체수평.결과 여단순OGD조상비,OGD+TAN-67조배액중적LDH수평명현하강,형광염색현시활세포증가사세포감소,차DOR단백표체증가;OGD+naltrindole조칙세포수손가중.차DOR단백표체감소.PKC억제제CHE능억제DOR격활후배액중LDH수평적하조.결론 DOR격동제가이항신경원양당박탈손상.길항DOR칙가중해손상.PKC가능삼여료DOR적신경보호작용.
Objective To investigate the effect of cortical 8-opioid receptor (DOR) on oxygen-glucose deprivation-induced (OGD-induced) neuronal injury. Methods Primary cultured cortical neurons incubated with selective DOR agonist (TAN-67) and antagonist (naltrindole) or PKC inhibitor (chelerythrine, CHE) were exposed to OGD. Lactate dehydrogenase (LDH) release was detected after 24 h reperfusion. The expression levels of DOR were measured by Western blot. Results Compared with OGD group, TAN-67 significantly decreased OGD-indueed LDH release, and increased the expression levels of DOR, while nahrindole aggravated neuronal injury and decreased the DOR protein expression. CHE could abolish the LDH down-regulation induced by TAN-67 plus OGD (P< 0.05, compared with TAN-67 treated group). Conclusions DOR activation protects neurons against OGD injury. PKC might take part in the neuroprotection pathways of DOR.