人参二醇组皂甙对正常和“缺血”诱导的大鼠大脑皮层神经元L-型钙通道的影响

Effects of panaxadiol saponins on the L type calcium channel of cortical neurons of rats in normal and“ischemia”

目的：研究人参二醇组皂甙（ＰＤＳ）对正常和“缺血”状态下大鼠大脑皮层神经元Ｌ－型钙通道的影响。方法：急性分离大鼠大脑皮层神经元建立体外“缺血”模型，用细胞贴附膜片钳单通道记录方法。结果：在“缺血”过程中，大鼠大脑皮层神经元Ｌ－型钙通道平均开放时间明显增加，并出现长达２０ｍｓ的长时程开放，平均关闭时间缩短，开放概率增加。ＰＤＳ１．５ｍｇ／ｍｌ可显著抑制正常和“缺血”诱导的Ｌ－型钙通道的开放，使其平均开放时间缩短，平均关闭时间延长，开放概率降低，此作用与经典钙通道阻断剂Ｖｅｒａｐａｍｉｌ相似，但作用稍弱。结论：ＰＤＳ可抑制正常和“缺血”诱导的大鼠大脑皮层神经元Ｌ－型钙通道开放，从而减少钙内流，对缺血脑细胞可能有保护作用。

Objective: To study the effects of panaxadiol saponins(PDS) on the L type calcium channel of cortical neurons of rats in normal and “ischemia”. Methods: Using acutely isolated cortical neurons of Wistar rats to estabilish the in vitro cerebral “ischemic model” and patch clamp technique of cell attached configulation. Results: The results indicated that the open time of L type calcium channel of rat cortical neurons was increased, at the same time, the close time decreased and the open state probability increased significantly during “ischemia”. The particular change was long lasting open (the open time was more than 20 ms). PDS ( 1.5 mg/ml) shorten the open time, prolong the close time and decrease the open state probablity in normal and “ischemia” like condition (P all<0.001). These results were consistent with calcium antagonist verapamil, but were less than that of verapamil. Conclusion: The experiment suggested that PDS inhibited the open of L type calcium channel in cortical neurons of rats in normal and “ischemia”, reduced the calcium inflow, and may protect brain from the ischemic injury.