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川芎嗪抗伤害性反应作用机制初探 被引量:5

Antinociceptive response mechanism of tetramethylpyrazine
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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.
出处 《中草药》 CAS CSCD 北大核心 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 )
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 tetramethylpyrazine (TMP) nociceptive response adenosine triphosphate (ATP) purine 2X (P2X) receptors prostaglandin E 2(PGE 2) substance P (SP)
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