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[摘要]
目的 研究苦参碱的镇痛作用部位及机制。方法 采用小鼠醋酸扭体法、热板法 ,观察用药后扭体反应数、舔后足潜伏期及脑组织 NO含量的变化。结果 苦参碱侧脑室注射 (icv) 0.25,0.5mg/ kg,ip或 iv 3.75 ,7.5 ,15 ,30mg/ kg均可显著减少小鼠扭体反应数 ,并呈量效关系ip与 iv同等剂量的苦参碱 ,对小鼠扭体反应的抑制程度多以iv为强 ,给药后各时段的 ip抗扭体半数有效量 (ED5 0 )均大于 iv抗扭体 ED5 0 ;ip苦参碱 7.5 ,30 mg/ kg可显著降低醋酸致痛小鼠脑组织 NO含量 ;进一步研究发现苦参碱延长小鼠舔后足潜伏期的作用可被氯化钙所拮抗 ,而被维拉帕米所增强。结论 苦参碱的镇痛作用部位在中枢 ,其镇痛作用可能与影响 Ca2+ 内流和减少 NO生成有关。
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[Abstract]
Object The site of analgesic action of matrine (Ma) and its mechanism were studied. Methods Adopting acetic acid writhing and hot plate test in mice, the changes of the number of writhing, the latencies of paw licking and the content of nitric oxide (NO) in the brain tissue after administration were recorded. Results Ma (0.25, 0.5 mg/kg, icv; 3.75, 7.5, 15, 30 mg/kg, ip or iv) could remarkably and dose-dependently reduce the numbers of writhing. When the same doses of Ma were given by ip and iv, its inhibitory effect on mouse writhing was more pronounced by iv than that by ip. The anti-writhing ED50?of Ma at any time after ip was larger than that after iv. Ma (7.5, 30 mg/kg, ip) could also obviously lowered the content of NO in the brain tissue of acetic acid writhing mouse. It was further found that the action of Ma that prolonged the latencies of paw licking could be antagonized by CaCl2and enhanced by verapamil. Conclusion The site of analgesic action of Ma is located in the central nervous system. Its mechanism of analgesic action may be related to its influence on the transmembrane influx of Ca2+?and reducing the output of NO.
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