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目的:应用氢过氧化枯烯(cumene hydroperoxide,CHP)作用于体外经全反式维甲酸(all-transretinoic acid,RA)分化培养的人神经母细胞瘤细胞SH-SY5Y,观察其对阿片受体介导环磷酸腺苷(cyclic a-denosine monophosphate,cAMP)含量的影响。方法:CHP预处理分化SH-SY5Y细胞后,通过吗啡的急性、慢性作用和纳洛酮(naloxone,NLX)阻断,观察腺苷酸环化酶激动剂Forsklin(Fs)诱导的胞内cAMP水平的变化。不同浓度的CHP作用于分化的SH-SY5Y细胞24 h,进行细胞内活性氧(reactive oxygen species,ROS)水平、丙二醛(malondialdehyde,MDA)含量检测、超氧化物歧化酶(superoxide dismutase,SOD)和过氧化氢酶(catalase,CAT)活性检测。结果:吗啡急性作用,抑制了Fs诱导的胞内cAMP含量的增加,CHP预处理吗啡急性作用的SH-SY5Y细胞,显著降低了吗啡对Fs诱导的胞内cAMP水平的抑制作用;吗啡长期作用,使Fs诱导的胞内cAMP水平恢复到正常;NLX阻断,使胞内cAMP水平进一步升高。CHP预处理吗啡长期作用和NLX阻断的SH-SY5Y细胞,使吗啡对Fs诱导的胞内cAMP水平降低。CHP引起SH-SY5Y细胞的氧化损伤,使细胞内ROS的水平上升,MDA含量增高及降低细胞内SOD和CAT的活力。结论:ROS使μ-阿片受体的功能受到损伤,其可能通过调节阿片受体介导的cAMP含量的变化而参与了吗啡依赖的机制。
AIM: To investigate the effect of cumene hydroperoxide (CHP) on human neuroblastoma SH-SY5Y cells differentiated by all-transretinoic acid (RA) Mediated cyclic a-denosine monophosphate (cAMP) content. Methods: After CHP preconditioning differentiated into SH-SY5Y cells, the intracellular cAMP level induced by the adenylate cyclase agonist Forsklin (Fs) was observed through the acute and chronic morphine treatment and the blockade of naloxone (NLX) The change. Different concentrations of CHP were applied to the differentiated SH-SY5Y cells for 24 h. The levels of reactive oxygen species (ROS), malondialdehyde (MDA), superoxide dismutase (SOD) ) And catalase (CAT) activity. RESULTS: The acute morphine treatment inhibited the increase of intracellular cAMP levels induced by Fs. Pretreatment with CHP pretreated SH-SY5Y cells induced by morphine significantly reduced the inhibitory effect of morphine on intracellular cAMP levels induced by Fs; long-term morphine treatment, Fs-induced intracellular cAMP levels returned to normal; NLX block, so that intracellular cAMP levels increased further. CHP pretreatment morphine long-term and NLX blocked SH-SY5Y cells, so morphine Fs-induced intracellular cAMP levels decreased. CHP caused oxidative damage of SH-SY5Y cells, increased intracellular ROS levels, increased MDA content and decreased intracellular SOD and CAT activity. Conclusion: ROS can impair the function of μ-opioid receptor, which may be involved in the morphine-dependent mechanism by regulating the opioid receptor-mediated changes of cAMP content.