激活δ-阿片受体可对抗原代培养神经元氧糖剥夺损伤

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。     

NO调控JNKs通路对鼠海马神经元保护作用研究

Background C-Jun N-terminal kinase (JNK) signaling pathway plays a critical role in cerebral ischemia. Although the mechanistic basis for this activation of JNK1/2 is uncertain, oxidative stress may play a role. The purpose of this study was to investigate whether the activation of JNK1/2 is associated with the production of endogenous nitric oxide. Methods Ischemia and reperfusion was induced by cerebral four-vessel occlusion (4-VO). Sprague–Dawley (SD) rats were divided into 6 groups: sham group, ischemia and reperfusion group, neuronal nitric oxide synthase (nNOS) inhibitor 7-Nitroindazole (7-NI) (Sigma St Louis, MO, USA) given group, inducible nitric oxide synthase (iNOS) inhibitor (AMT) (Sigma) given group, sodium chloride control group and 1% dimethyl sulfoxide (DMSO) control group. The levels of protein expression and phospho-JNK1/2 were detected by western blot and the survival hippocampus neurons in CA1 zone were observed by cresyl violet (CV) staining. Results The study illustrated two peaks of JNK1/2 activation occurred at 30 min and 3 days during reperfusion. 7-NI inhibited JNK1/2 activation during the early reperfusion, whereas AMT preferably attenuated JNK1/2 activation during the later reperfusion. At same time, the results also showed that administration of 7-NI and AMT can decrease ischemia/Reperfusion (I/R)-induced neuronal loss in hippocampal CA1 region. Conclusions JNK1/2 activation is associated with endogenous nitric oxide (NO) in response to ischemic insult.     

全身麻醉药对发育期大脑的影响:毒性作用还是保护作用

<正>大部分婴幼儿手术需要在全身麻醉(简称全麻)下进行,但全麻药在产生麻醉效果的同时,也产生明显的非麻醉作用,可能主要对发育期大脑可能有神经毒性作用[1-2]。对于全麻药麻醉作用的机制,至今还不甚清楚,目前可以肯定的是,全麻药通过兴奋γ氨基丁酸(γ-aminobutyric acid,GABA)受体或抑制N-甲基-D-天冬氨酸(N-methyl-D-aspartate,NMDA)受体而发挥全麻作用。由于GABA受体、NMDA受体介导的生理过程在哺乳动物大脑发育过程     

针刺治疗足下垂型腰椎间盘突出症临床研究

目的：探讨针刺治疗足下垂型腰椎间盘突出症的临床疗效。方法：将90例足下垂型腰椎间盘突出症患者按随机数字表法分为对照组和观察组,观察组采用针刺治疗,对照组采用牵引治疗,治疗后比较两组疗效、足背肌力及随访后JOA评分情况。结果：治疗后观察组有效率为93.3%,对照组有效率为84.4%,两组比较差异有统计学意义（P〈0.05）。治疗后观察组肌力Ⅲ级达12例,Ⅳ级19例,Ⅴ级14例,对照组治疗后肌力Ⅲ级达21例,Ⅳ级10例,Ⅴ级6例,观察组肌力改善情况明显优于对照组（P〈0.05）。随访1 a后腰椎JOA评分观察组明显高于对照组,差异有统计学意义（P〈0.05）。结论：针刺治疗足下垂型腰椎间盘突出症疗效显著,且能提高患者的肌力。     

瞬时受体电位8型的功能结构及其化学调节剂的研究进展

瞬时受体电位8型(transient receptor potential melastatin-related 8，TRPM8)是一种非选择性钙离子通道，其功能异常或缺失会导致多种疾病。TRPM8参与生物体的体温调节、肿瘤、炎症、疼痛和哮喘等生理及病理活动，特别是在肿瘤治疗过程中，TRPM8常被用作治疗的潜在靶点。大部分化学调节剂是通过影响细胞内Ca²⁺浓度平衡来激活TRPM8通道。本文对TRPM8通道的结构、功能及其对不同疾病的调节作用等进行归纳及分析，为TRPM8作为临床治疗及新药开发靶点提供借鉴。