中文摘要：

目的：利用RNAi重组腺病毒下调第10号染色体同源丢失性磷酸酶张力蛋白基因（phosphata-se and tensin homology deleted on chromosome ten, PTEN）的表达，探讨PTEN基因是否参与偏头痛的病理过程及其对三叉神经节内N-甲基-D-天冬氨酸受体l亚基（N-methyl-D．aspartatereceptor1，NMDAR1，简写NR1）和一氧化氮（nitricoxide，NO）的影响。方法：SD大鼠分成4组：假手术组（Sham组，n=12）；硝酸甘油模型组（NTG组，n=12）；PTEN基因下调组（AdR．siPTEN组，n=12）：Ad-RFP非特异siRNA处理空载体对照组（Ad．RFP组，n=12）。将重组腺病毒立体定向注射入大鼠三叉神经节内，一周后通过皮下注射NTG建立偏头痛大鼠模型，分别于NTG注射前及注射后15分钟、30分钟、1、2、4小时观察大鼠痛阈变化，同时检测各组大鼠三叉神经节NR1和NO的差异。结果：AdR-siPTEN腺病毒可下调三叉神经节PTEN基因的表达。与Ad．RFP组相比，AdR-siPTEN组的偏头痛大鼠痛阈明显增高，并且三叉神经节内NRl表达及NO合成明显减少。结论：PTEN基因参与调节偏头痛的病理过程，下调PTEN基因可减轻NTG诱导的偏头痛大鼠模型对机械性刺激的反应，其机制可能是下调PTEN引起NR1表达量减低，继而引起NO含量降低所致。

英文摘要：

Objective： To employ the recombinant adenovirus AdR-siPTEN to knock down the gene of NMDA receptor NR1 subunit, to examine whether PTEN can modulate the pathological mechanism of migraine. Methods： Sprague-Dawley rats were randomly divided into 4 groups： Sham group （n = 12）; NTG group （n = 12）; AdR-siPTEN group （n = 12）; Ad-RFP group （n = 12）. One week after intraparenchymal administration of AdR-siPTEN into trigeminal ganglion, NTG was injected subcutaneously. The mechanic- al nociceptive thresholds before and at 15 rain, 30 rain, 1 h, 2 h and 4 h after NTG was evaluated, The change of NR1 expression and NO production of trigeminal ganglion were investigated. Results： The PTEN gene of trigeminal ganglion was down-regulated by the localized injection of AdR-siPTEN, which significantly increased the mechanical nociceptive thresholds and attenuated the NR1 expression and NO production of trigeminal ganglion in NTG-induced rats. Conclusion： PTEN may modulate the pathological mechanism of migraine. The PTEN gene down-regulation can reduce NTG-induced mechanical hypersensitivity. The mechanism related to the decreased NR1 expression and NO production.