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兴奋性氨基酸类神经毒剂与粉防己碱（Ｔｅｔ）共同作用于原代培养胎鼠大脑皮层神经元２４ｈ，发现１０－７，１０－６ｍｏｌ·Ｌ－１Ｔｅｔ明显降低谷氨酸（Ｇｌｕ），β－Ｎ－ｏｘａｌｙｌａｍｉｎｏ－Ｌ－ａｌａｎｉｎｅ（ＢＯＡＡ）和β－Ｎ－ｍｅｔｈｙｌａｍｉｎｏ－Ｌ－ａｌａｎｉｎｅ（ＢＭＡＡ）导致的培养液乳酸脱氢酶（ＬＤＨ）活性增高，细胞形态损害减轻，细胞数量增加。对ＮＭＤＡＡ介导的神经元损伤改变无影响。提示Ｔｅｔ对某些Ｇｌｕ类神经毒剂引起的胎鼠大脑皮层神经元损伤有一定保护作用，其机制可能是抑制细胞膜Ｎａ＋通道开放，阻止膜去极化而影响电压依赖性Ｃａ２＋通道启动。对ＮＭＤＡ受体可能亦有一定作用。
Excitatory amino acid neurotoxic agents combined with tetrandrine (Tet) in primary cultured fetal rat cerebral cortical neurons 24h and found 10-7,10-6mol · L-1Tet significantly reduced glutamate (Glu), β- Lactate dehydrogenase (LDH) activity in culture medium induced by N-oxalylamino-L-alanine (BOAA) and β-N-methylamino-L-alanine (BMAA) increased, cell morphology damage and cell number increased. No effect on NMDAA-mediated changes in neuronal damage. It is suggested that Tet may protect neurons of fetal rat cerebral cortex induced by some neurotoxic agents of Glu. The mechanism may be that the inhibition of membrane Na + channel opening and the depolarization of membrane may affect the activation of voltage-dependent Ca 2+ channel. NMDA receptors may also have a role.