Effects of ginsenoside Rd and decursinol on the neurotoxic responses induced by kainic acid in mice
Effects of ginsenoside Rd and decursinol on the neurotoxic responses induced by kainic acid in mice
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DOI：
10.1055/s-2003-38475
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发表时间：
2003-03-01
期刊：
影响因子：
2.7
通讯作者：
Suh, HW
中科院分区：
文献类型：
--
作者：
Lee, JK;Choi, SS;Suh, HW
在本研究中，我们研究了G-Rd（G-Rd）和decursinol（DC）对海人酸（KA）诱导的各种神经毒性反应的影响。C. v.）的一个例子在ICR小鼠中。人参总皂苷（GTS）抑制KA（0.5 μ g）诱导的致死毒性，呈剂量依赖性。此外，G-Rd，GTS的一个组成部分，也衰减KA诱导的致死毒性，以及DC预处理口服30分钟。在ICR小鼠，KA（0.1马克杯）在海马引起的神经毒性损伤显着集中在CA 3锥体神经元。G-Rd和DC对海马CA 3区锥体细胞死亡无影响。在一项免疫组织化学研究中，KA显著增加海马区磷酸化ERK和减少磷酸化CREB。G-Rd和DC部分减弱了磷酸化ERK的增加和磷酸化CREB蛋白水平的降低。然而，DC加强KA诱导的海马c-Fos和c-Jun蛋白水平的增加。因此，我们的研究结果表明，ERK的磷酸化或CREB蛋白的去磷酸化可能在调节KA诱导的致死毒性中发挥重要作用，而KA诱导的海马CA 3区细胞死亡可能不是直接介导的ERK磷酸化和CREB磷酸化在小鼠中。
In the present study, we examined the effects of ginsenoside Rd (G-Rd) and decursinol (DC) on various neurotoxic responses induced by kainic acid (KA) administered intracerebroventricularly (i. c. v.) in ICR mice. Ginseng total saponin (GTS) inhibited the KA (0.5 mug)-induced lethal toxicity in a dose-dependent manner. Furthermore, G-Rd, a component of GTS, also attenuated the KA-induced lethal toxicity as well as DC pretreated orally for 30 min. In ICR mouse, neurotoxic damage induced by KA (0.1 mug) in the hippocampus was markedly concentrated in the CA3 pyramidal neurons. G-Rd and DC did not affect the pyramidal cell death in CA3 hippocampal region. In an immunohistochemical study, KA dramatically increased phospho-ERK and decreased phospho-CREB in the hippocampal area. G-Rd and DC attenuated, in part, the increased phospho-ERK and the decreased phospho-CREB protein levels. However, DC potentiated the increased c-Fos and c-Jun protein levels in the hippocampus induced by KA. Thus, our results suggest that the phosphorylation of ERK or the dephosphorylation of CREB protein may play a major role in the regulation of lethal toxicity induced by KA, whereas cell death in the hippocampal CA3 region induced by KA administered i.c.v. may not be directly mediated by ERK phosphorylation and CREB phosphorylation in the mouse.