CAJ | 학술논문

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iv3.75，7.5，15，30mg/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(ED50)均大于iv抗扭体ED50；ip苦参碱7.5，30mg/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。
목적 연구고삼감적진통작용부위급궤제。방법 채용소서작산뉴체법、열판법，관찰용약후뉴체반응수、첨후족잠복기급뇌조직NO함량적변화。결과 고삼감측뇌실주사(icv)0.25，0.5mg/kg，ip혹iv3.75，7.5，15，30mg/kg균가현저감소소서뉴체반응수，병정량효관계；ip여iv동등제량적고삼감，대소서뉴체반응적억제정도다이iv위강，급약후각시단적ip항뉴체반수유효량(ED50)균대우iv항뉴체ED50；ip고삼감7.5，30mg/kg가현저강저작산치통소서뇌조직NO함량；진일보연구발현고삼감연장소서첨후족잠복기적작용가피록화개소길항，이피유랍파미소증강。결론 고삼감적진통작용부위재중추，기진통작용가능여영향Ca2+내류화감소NO생성유관。
Object The site of analgesic action of matrine (Ma) and itsmechanism 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 CaCl2 and 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.