激活δ-阿片受体可对抗原代培养神经元氧糖剥夺损伤  

δ-opioid receptors protect neurons against neuronal injury induced by oxygen-glucose deprivation

作　　者：李名伟[1] 朱敏[1] 田雪松[1] 区晓敏[1] 夏萤[2,3] 郭景春[1] 

机构地区：[1]复旦大学医学神经生物学国家重点实验室,上海200032 [2]上海市针灸经络研究中心,上海201203 [3]美国耶鲁大学医学院

出　　处：《复旦学报（医学版）》2009年第4期389-393,共5页Fudan University Journal of Medical Sciences

摘　　要：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-67、拮抗剂naltrindole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24h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。Objective To investigate the effect of cortical 3-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-induced 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.

关 键 词：神经元 氧糖剥夺 Δ-阿片受体 神经保护 

分 类 号：R338[医药卫生—人体生理学]