Saikosaponin a mediates the anticonvulsant properties in the HNC models of AE and SE by inhibiting NMDA receptor current and persistent sodium current.

Saikosaponin a mediates the anticonvulsant properties in the HNC models of AE and SE by inhibiting NMDA receptor current and persistent sodium current.
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柴胡皂苷 a 通过抑制 NMDA 受体电流和持续钠电流介导 AE 和 SE 的 HNC 模型的抗惊厥特性

DOI:
10.1371/journal.pone.0050694
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发表时间:
2012
期刊:
影响因子:
3.7
通讯作者:
Xing JL
Xing JL
中科院分区:
综合性期刊3区
文献类型:
--
作者:
Yu YH;Xie W;Bao Y;Li HM;Hu SJ;Xing JL

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Epilepsy is one of the most common neurological disorders, yet its treatment remains unsatisfactory. Saikosaponin a (SSa), a triterpene saponin derived from Bupleurum chinensis DC., has been demonstrated to have significant antiepileptic activity in a variety of epilepsy models in vivo. However, the electrophysiological activities and mechanisms of the antiepileptic properties of SSa remain unclear. In this study, whole-cell current-clamp recordings were used to evaluate the anticonvulsant activities of SSa in the hippocampal neuronal culture (HNC) models of acquired epilepsy (AE) and status epilepticus (SE). Whole-cell voltage-clamp recordings were used to evaluate the modulation effects of SSa on NMDA-evoked current and sodium currents in cultured hippocampal neurons. We found that SSa effectively terminated spontaneous recurrent epileptiform discharges (SREDs) in the HNC model of AE and continuous epileptiform high-frequency bursts (SE) in the HNC model of SE, in a concentration-dependent manner with an IC50 of 0.42 µM and 0.62 µM, respectively. Furthermore, SSa significantly reduced the peak amplitude of NMDA-evoked current and the peak current amplitude of INaP. These results suggest for the first time that the inhibitions of NMDA receptor current and INaP may be the underlying mechanisms of SSa’s anticonvulsant properties, including the suppression of SREDs and SE in the HNC models of AE and SE. In addition, effectively abolishing the refractory SE implies that SSa may be a potential anticonvulsant candidate for the clinical treatment of epilepsy.
DOI: 10.1016/s0031-9422(99)00073-4
发表时间: 1999-07-01
期刊: PHYTOCHEMISTRY
影响因子: 3.8
作者:
Ono, M;Yoshida, A;Nohara, T
通讯作者: Nohara, T
DOI: 10.1212/wnl.43.8.1473
发表时间: 1993-08-01
期刊: NEUROLOGY
影响因子: 9.9
作者:
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通讯作者: HAUSER, WA
DOI: 10.1016/s0006-8993(99)02035-1
发表时间: 1999-12-18
期刊: BRAIN RESEARCH
影响因子: 2.9
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DOI: 10.1152/jn.1987.57.3.869
发表时间: 1987-03-01
影响因子: 2.5
作者:
MODY, I;LAMBERT, JDC;HEINEMANN, U
通讯作者: HEINEMANN, U
DOI: 10.1073/pnas.080071697
发表时间: 2000-05-09
影响因子: 11.1
作者:
Churn, SB;Sombati, S;DeLorenzo, RJ
通讯作者: DeLorenzo, RJ