摘要
目的：研究新的桂皮酰胺类化合物３，４二氯苯丙烯酰另丁胺（简称ＡＥＤ８８０１）对分离的神经细胞内游离钙离子的影响。方法：采用Ｃａ２＋指示剂Ｆｕｒａ２作为细胞内钙离子的荧光探针，利用ＲＦ－５０００型双波长荧光分光光度计检测分离的神经细胞内游离钙离子及其变化，并观测ＡＥＤ８８０１对静息态细胞内钙离子、高Ｋ＋去极化状态及ＮＭＤＡ刺激情况下的细胞内钙离子变化的影响。结果：在静息状态下，细胞内钙离子浓度［Ｃａ２＋］ｉ为（２０６．５±１１．２）μｍｏｌ·Ｌ－１，高Ｋ＋去极化及ＮＭＤＡ刺激后［Ｃａ２＋］ｉ均增加。ＡＥＤ８８０１０和１００μｍｏｌ·Ｌ－１可以轻度降低静息态［Ｃａ２＋］ｉ，但无统计学意义（Ｐ＞０．０５），对高Ｋ＋去极化引起的［Ｃａ２＋］ｉ增加无明显的影响（Ｐ＞０．０５），而可降低由于ＮＭＤＡ引起的［Ｃａ２＋］ｉ增加，以１０μｍｏｌ·Ｌ－１和１００μｍｏｌ·Ｌ－１作用明显，与对照组比较Ｐ＜０．０５和Ｐ＜０．０１。结论：ＡＥＤ８８０１对电压依赖性的离子通道无明显的影响。
OBJECTIVE: To
investigate the influence of 3,4dichlorophenylsec.butylamine (AED8801),a new derivative of
cinnamamides on the intracellular free calcium in rat isolated brain cells. METHOD: Using
Ca2+sensitive fluorescent indicator,Furo2 and a fluorescence detector (Shimadzu
RF5000,Japan),intracellular free Ca2+(]i) was measured.The influence of AED8801 on the i
resting status,depolarization induced by KCl and the addition of NmethylDaspartate (NMDA)
were observed. RESULTS: The average intracellular free Ca2+ concentration in resting status
was 206.5+11.2 molL-1,depolarization induced by KCl and NMDA can increase i respectively.3,
4dichlorophenylpropenoylsec.butylamine 1,10 and 100molL-1 decreased the resting status i,but
no statistic significance (P>0.05) inhibited the NMDAinduced i elevation (P<0.05,P<0.01),and
did not decrease the high extracellular K+induced 2+]i elevation (P>0.05). CONCLUSION:
AED8801 can inhibit the Ca2+ channel of receptordependent,but can not inhibit the Ca2+
channel of voltagedependent.
出处
《中国药学杂志》
EI
CAS
CSCD
北大核心
1999年第6期372-374,共3页
Chinese Pharmaceutical Journal
基金
国家自然科学基金
关键词
神经细胞
钙离子
脑缺血
AED8801
dichlorophenylpropenoylsec.butylamine,intracellular
free Ca2+ concentration,cerebral ischemia injury
