目的 :本实验观察炎症痛和针刺镇痛时

大鼠中脑导水管周围灰质 (PAG)部位I型白细胞介素 1受体基因 (IL 1RImRNA)表达的变化。方法 :实验分正常组、炎症痛组、假电针组、电针组。正常对照组大鼠脚掌注射生理盐水

炎症痛各组大鼠脚掌注射 2 %角叉菜胶 ( 1 0 0 μL)造成炎症痛模型。在角叉菜胶注射 3hr后大鼠处于一种稳定的痛敏状态。电针组大鼠于造模前电针将致炎侧“足三里”和“昆仑”穴 3 0min

假电针组大鼠给予同样处理但不通电。实验采用原位杂交技术

观察脚掌注射角叉菜胶 3hr后大鼠中脑导水管周围灰质 (PAG)部位IL 1RImRNA表达的变化及针刺对其的影响。结果 :致炎后 3hr大鼠痛阈显著降低

大鼠PAG部位的IL 1RImRNA表达显著增加

假电针组大鼠该部位的IL 1RImRNA表达与炎症痛组相比无显著变化

而电针组大鼠该部位的IL 1RImRNA阳性细胞数与假电针组相比显著减少。结论 :炎症痛可引起大鼠PAG部位的IL 1RImRNA表达增加

而电针镇痛则抑制炎症痛引起的大鼠PAG部位IL 1RImRNA表达Objective: The aim of the present study was to observe the changes of expression of IL-1R(receptor)-I mRNA in rat periaqueductal gray after peripheral inflammation and electroacupuncture (EA) analgesia. Methods: Twenty-four SD rats were evenly divided into normal group

inflammation group

sham EA group and EA group. Rats of normal group received an intraplantar injection of 100 μL normal saline

and those of inflammation group

sham EA group or EA group received an intraplantar injection of 100 μL carrageenan (2%

100 μL). EA stimulation (4～60 Hz

1～2～3 mA

every 10 min for each current strength) was applied to unilateral "Zusanli" (ST 36) and "Kunlun" (BL 60) 3 hr after intraplantar injection of carrageenan. Sham EA was performed in the same way as EA except no EA was given. The expression of IL-1RI mRNA in rat periaqueductal gray following peripheral carrageenan inflammation was measured using in situ hybridization technique. The paw withdraw latency (PWL) was detected before and after different treatment. Results: Three hours after injection of carrageenan

PWL values of normal control

inflammation

sham EA and EA groups were 13.34±2.11 sec

2.03±0.16 sec

2.27±0.18 sec and 5.16±1.26 sec respectively; while compared with inflammation and sham EA groups

PWL of EA group increased significantly (P<0.05). Following carrageenan inflammation

the expression of IL-1RI mRNA in rat periaqueductal gray was significantly increased (positive reaction cells: 60.86±7.38

vs control group: 13.67±2.74

P< 0.001). Sham EA did not influence the expression of IL-1RI mRNA (61.45±6.49 positive cells)

but EA could significantly inhibit the expression of IL-1RI mRNA (37.08±6.36 positive cells

P<0.05

vs inflammation and sham EA groups) in the same central region in carrageenan inflammatory rat. Conclusion: Carrageenan inflammation increases the expression of IL-1RI mRNA in rat periaqueductal gray

and EA analgesia could significantly inhibit the expression of IL-1RI mRNA in carrageenan inflammatory rats.