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目的:研究缺氧对大鼠大脑皮层神经元L型钙通道的影响和人参二醇皂苷(PDS)保护的机制.方法:细胞贴附膜片钳法.结果:缺氧致钙通道开放时间由(285±021)ms增加到(91±10)ms(P<001),开放概率由(0047±0008)增加到(0165±0025)(P<001).PDS(15g·L-1)抑制正常和缺氧时钙通道的开放[开放时间分别由(223±047)ms和(91±10)ms减到(103±025)ms和(21±04)ms,开放概率分别由(0043±0006)和(0165±0025)减到(0012±0004)和(0021±0009)].结论:缺氧可明显开放大鼠大脑皮层神经元L型钙通道,PDS可有效抑制之,此为其保护缺氧脑的机制之一.
Objective: To study the effects of hypoxia on L-type calcium channels in rat cortical neurons and the mechanism of PDS protection. Methods: Cell patch patch clamp method. Results: The opening time of hypoxia induced calcium channel increased from (285±021)ms to (91±10)ms (P<001), and the open probability was (0047±0). 008) increase to (0165±0025) (P<001). PDS (15g·L-1) inhibits the opening of calcium channels during normal and hypoxia [open time from (223±047)ms and (91±10)ms] to (1) 03±025)ms and (21±04)ms, the open probability is reduced from (0043±0006) and (0165±0025) to (0012±) 0004) and (0021±0009)]. CONCLUSION: Hypoxia can significantly open up L-type calcium channels in rat cerebral cortical neurons. PDS can effectively inhibit it, which is one of the mechanisms of hypoxic brain protection.