刘庆华,刘雅静.马棘根乙醇提取物舒张小鼠气道平滑肌[J].中南民族大学学报自然科学版,2021,40(2):131-137
马棘根乙醇提取物舒张小鼠气道平滑肌
Relaxation effect of ethanol extract from Indigogera pseudotinctoria Mats. root on airway smooth muscle in mice
  
DOI:10.12130/znmdzk.20210204
中文关键词: 马棘  气道平滑肌  细胞内钙  离子通道
英文关键词: Indigogera pseudotinctoria Mats.  airway smooth muscle  intracellular Ca2+  ion channel
基金项目:国家自然科学基金资助项目(31571200)
作者单位
刘庆华 中南民族大学 生命科学学院 & 医学生物研究所 & 武陵山区特色资源植物种质保护与利用湖北省重点实验室武汉430074 
刘雅静 中南民族大学 生命科学学院 & 医学生物研究所 & 武陵山区特色资源植物种质保护与利用湖北省重点实验室武汉430074 
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中文摘要:
      为研究马棘根乙醇提取物(EEIP)逆转小鼠气道平滑肌(ASM)的收缩及其机制,利用张力测量系统测量小鼠气管环张力,MTT法检测EEIP对16HBE细胞存活率的影响,肺切片技术测量肺内支气管的收缩与舒张,钙成像系统测量ASM细胞内Ca2+水平,动物肺功能仪测量活体小鼠呼吸系统阻力(Rrs).结果表明:EEIP能够完全逆转ACh诱发的小鼠离体气管环和肺内支气管的收缩,且呈剂量依赖性,但不影响静息状态气管环张力;EEIP还能阻断ACh引起的稳态细胞内Ca2+升高.此外,ACh诱发的收缩能够被L型电压依赖性钙通道(LVDCC)和钙库操纵性钙通道(SOCC)两种通透Ca2+通道的选择性阻断剂部分抑制,剩余部分被EEIP所阻断.在活体小鼠,EEIP能够降低ACh引起的Rrs升高.引起最大舒张浓度的EEIP对16HBE细胞活性无影响因此EEIP可抑制LVDCC和SOCC,并介导Ca2+内流停止,细胞内Ca2+降低,这是EEIP逆转ASM收缩的机制,这种机制也存在于活体状态.故马棘和EEIP可用于开发新的气管扩张剂.
英文摘要:
      To investigate the mechanism of ethanol extract of Indigogera pseudotinctoria Mats. root (EEIP) in reversing the contraction of mouse airway smooth muscle (ASM), the tension of mouse tracheal ring was measured by a tension measurement system, the viability rate of 16HBE cells was measured by the MTT method, the contraction and relaxation of intrapulmonary bronchi were measured by the lung slice technology, the intracellular Ca2+ level in ASM cells was measured by a calcium imaging system, and the resistance of respiratory system (Rrs) was measured in vivo with an animal pulmonary function measurement system. The results indicated that EEIP could completely reverse ACh-induced contraction of mouse tracheal rings and intrapulmonary bronchi in a dose-dependent manner; however, it did not affect the tension of resting tracheal rings. EEIP blocked ACh-induced steady-state elevations of Ca2+. In addition, ACh-induced contraction was partially inhibited by selective blockers of both L-type voltage-dependent Ca2+ channel (LVDCC) and store-operated Ca2+ channel (SOCC), which permeated Ca2+. The remaining contraction was blocked by EEIP. EEIP reduced ACh-induced Rrs elevations in vivo. The maximum relaxation concentration of EEIP had no effect on 16HBE cell viability. So EEIP inhibited LVDCC and SOCC, mediated Ca2+ influx and decreased the intracellular Ca2+ concentration, as a result of the EEIP-reversed ASM contraction mechanism. This mechanism was also exhibited in vivo. Therefore, Indigogera pseudotinctoria Mats. and EEIP could be used to develop new bronchodilators.
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