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The effect of Toki‐Shakuyaku‐San (TJ‐23) was examined on various models of brain damage in vitro. TJ‐23 (10 mg/mL) significantly protected striatal slices from dysfunction induced by high K+ and BAY K‐8644 but not from that by L‐glutamate and N‐methyl‐D‐aspartate, an effect which was similar to that of nifedipine, a Ca2+ antagonist. The present findings, therefore, raised the possibility that TJ‐23 expressed a neuroprotective action on hypoxia/ischaemia‐induced brain damage by inhibiting an excess Ca2+ entry through voltage‐gated Ca2+ channels.
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Kataoka et al. (1993) studied this question.
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