中文摘要：

目的：评价鞘内注射2-PMPA对大鼠慢性炎性痛的影响。方法雄性SD大鼠24只，4～6月龄，体重200～250 g ，采用随机数字表法，将其分为3组（ n＝8）：生理盐水组（NS组）、完全弗氏佐剂组（CFA组）和N-乙酰天冬氨酰谷氨酸肽酶抑制剂2-PMPA组。采用左侧足底注射CFA 100μl的方法制备大鼠慢性炎性痛模型；2-PMPA组给予CFA后即刻鞘内注射2-PMPA 100μg ，其它2组给予等容量生理盐水，1次/d ，连续3 d。分别于注射CFA前（基础状态，T1）和最后一次给予2-PMPA后（T2）测定热缩足潜伏期（TWL ）和机械缩足反应阈（PWT ），然后处死大鼠，取L4，5节段脊髓组织，采用Western blot法测定NR2B表达。结果与NS组比较，CFA组和2-PMPA组T2时TWL和 PWT均降低，脊髓NR2B表达上调（ P＜0.05）；与CFA组比较，2-PMPA组T2时TWL和PWT均升高，脊髓NR2B表达下调（ P＜0.05）。结论鞘内注射2-PMPA可减轻大鼠慢性炎性痛，其机制与抑制脊髓水平NR2B表达有关。

英文摘要：

Objective To evaluate the effects of intrathecal 2-PMPA on chronic inflammatory pain in rats . Methods Twenty four male Sprague-Dawley rats ,aged 4-6 months ,weighing 200-250 g ,were randomly divided into 3 groups （n=8 each） using a random number table ：normal saline （NS） group ,complete Freund′s adjuvant （CFA ） group and N-acetylaspartylglutamate peptidase inhibitor 2-PMPA group （group 2-PMPA ） . Chronic inflammatory pain was induced by injecting 100μl of CFA into the plantar surface of the left hindpaw .Immediately after injection of CFA ,2-PMPA 100 μg was injected intrathecally once a day for 3 consecutive days in group 2-PMPA ,while the equal volume of NS was given instead of 2-PMPA in NS and CFA groups .The paw withdrawal latency to thermal nociceptive stimulus （TWL ） and paw withdrawal threshold （PWT ） to von Frey filament stimulation were measured before injection of CFA （baseline ,T1 ） and after the last injection of CFA （T2 ） .Then the rats were sacrificed and the L4 ,5 segments of the spinal cord were removed for determination of NR2B expression by Western blot .Results Compared with group NS ,TWL and PWT were significantly decreased at T2 and the expression of NR2B was up-regulated in CFA and 2-PMPA groups （ P〈0.05 ） .Compared with group CFA ,TWL and PWT were significantly increased at T2 and the expression of NR2B was down-regulated in group 2-PMPA （ P〈0.05） .Conclusion Intrathecal 2-PMPA can alleviate CFA-induced chronic inflammatory pain in rats ,and inhibition of NR2B expression in the spinal cord is involved in the mechanism .