川芎嗪抗伤害性反应作用机制初探  

Antinociceptive response mechanism of tetramethylpyrazine

作　　者：梁尚栋[1] 高云[1] 穆松牛[1] 许宝华[1] 徐昌水[1] 

机构地区：[1]江西医学院生理教研室,江西南昌330006

出　　处：《中草药》2005年第3期396-398,共3页Chinese Traditional and Herbal Drugs

基　　金：国家自然科学基金项目 (3 0 2 60 0 3 0 )

摘　　要：目的　观察川芎嗪(TMP)对嘌呤2 X(P2 X)受体激动剂[三磷酸腺苷(ATP)和α,β-亚甲三磷酸腺苷(α,β- me ATP) ]、前列腺素E2 (PGE2 )及P物质(SP)所致大鼠足底急性伤害性反应的影响。方法　通过大鼠痛行为反应确定局部应用TMP对ATP等P2 X受体激动剂、PGE2 及SP所致大鼠足底急性伤害性反应和足底炎症水肿的影响。结果　TMP (10 mm ol/L )明显抑制ATP (1μm ol/L )或α,β- m e ATP (0 .6μm ol/L )引起的大鼠足底急性伤害性反应。TMP(10 m mol/L)可抑制PGE2 (5 μmol/L)或α,β- me ATP(0 .2 μm ol/L)加PGE2 (5 μmol/L )引起的伤害性反应。TMP (10 m mol/L )不影响α,β- me ATP (0 .2μmol/L )加SP (10μmol/L )引起的伤害性反应。TMP对PGE2 、SP或α,β- m e ATP分别加PGE2 或SP引起的大鼠足底炎症水肿无明显影响。结论　TMP主要通过抑制P2 X受体兴奋介导的伤害性信息传递产生抗伤害性反应作用。Objective To observe the effects of tetramethylpyrazine (TMP) on acute nociception in rat hindpaw induced by purine 2X (P2X) receptor agonists, such as adenosine triphosphate (ATP) and α, β-meATP, prostaglandin E 2 (PGE 2), and substance P (SP). Methods The effects of TMP administered intraplantarlly on the acute nociception induced by P2X receptor agonists, PGE 2, or SP in the rat hindpaw were investigated by the method of the behavioral study. Results TMP (10 mmol/L) significantly depressed the acute nociception induced by ATP (1 μmol/L) or α, β-meATP (0.6 μmol/L) in the rat hindpaw. TMP (10 mmol/L) could inhibit the acute nociception induced by PGE 2 (5 μmol/L) or α, β-meATP (0.2 μmol/L) coinjected with PGE 2 (5 μmol/L). TMP (10 mmol/L) could not affect the acute nociception induced by α, β-meATP (0.2 μmol/L) coinjected with SP (10 μmol/L). TMP could not obviously affect the inflammatory edema in rat hindpaw induced by the local administration of PGE 2, SP, or α, β-meATP coinjected with PGE 2 or SP individually. Conclusion The antinociceptive effects of TMP may mainly be associated with inhibiting the transmission of nociceptive information mediated by P2X receptor activation.

关 键 词：川芎嗪 伤害性反应 三磷酸腺苷 嘌呤2X受体 前列腺素E2 P物质 

分 类 号：R339.11[医药卫生—人体生理学] R285.5[医药卫生—基础医学]