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贝母辛平喘作用及机制研究 被引量:37

Antiasthmatic mechanism of peimisine in Fritillaria monantha
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摘要 目的探讨彭泽贝母有效成分贝母辛平喘作用及机制。方法在离体器官水平,采用气管条浴槽实验方法,观测不同浓度的贝母辛对乙酰胆碱(Ach)、组胺(His)、CaCl2、β受体阻断剂、一氧化氮合酶抑制剂5种刺激因素诱发的气管平滑肌收缩的影响。结果贝母辛(0.046、0.092 mmol/L)使Ach诱发的大鼠、豚鼠气管平滑肌的EC50增大。贝母辛(0.092 mmol/L)对His的EC50无影响。贝母辛(0.092 mmol/L)对CaCl2致气管平滑肌收缩的EC50均无显著性差异。贝母辛3个剂量对Ach引起的气管平滑肌细胞内钙的释放具有显著的抑制作用(P<0.05、0.01、0.001),且具有剂量依赖关系;但对细胞外钙的内流均无明显抑制作用。与普萘洛尔+DMSO组比较,普萘洛尔+贝母辛组对气管平滑肌张力无降低作用,加入L-NAME后,贝母辛组3个剂量均未能抑制气管平滑肌的收缩。结论贝母辛通过作用于M受体、兴奋β受体和拮抗内钙释放,促进生成和释放一氧化氮从而舒张气管平滑肌,实现平喘的作用。 Objective To approach the antiasthmatic mechanism of peimisine in Fritillaria monatha. Methods To observe the effect of peimisine in the different concentration on the tracheal smooth muscle contraction in vitro organ induced by Ach, His, β-receptor, CaCl2, Pro, in nitricoxide synthase catastaltica. Results Peimisine (0. 046 and 0. 092 mmol/L) made the EC50 induced by Ach increased. The EC20 of peimsine (0. 092 mmol/L) was not changed by His;The EC50 of peimisine (0. 092 mmol/L) was not significantly different to tracheal smooth muscle contraction induced by CaCl2 . Three dosages of peimisine had significant inhibition on the release of intracellular calcium induced by CaCl2 (P 〈0. 05, 0.01, and 0. 001) in a dose-dependent manner. But extracellular calcium influx was not significantly inhibited. Comparing with the L-NAME+dissolvant group, three dosages of peimisine couldn't restrain the contraction and had no significant difference. Conclusion Peimisine could affect M-receptor, excit β-receptor, restrain the release of internal calcium, and promote to releaseing nitrogen monoxidum in order to relax tracheal smooth m'uscle and relieve asthma.
出处 《中草药》 CAS CSCD 北大核心 2009年第4期597-601,共5页 Chinese Traditional and Herbal Drugs
基金 国家自然科学基金重点项目(30160097)
关键词 贝母辛 气管平滑肌 平喘 peimisine tracheal smooth muscle antiasthmatic
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