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目的：观察具有较强钙调素拮抗活性的双苄基异喹啉类化合物Ｅ６ 对缺血性神经细胞损伤的保护作用。方法：采用ＮａＣＮ 加缺糖引起肾上腺髓质瘤细胞（ＰＣ１２ 细胞株）损伤和谷氨酸（ｇｌｕｔａｍａｔｅ，Ｇｌｕ） 引起乳大鼠脑皮质神经细胞损伤模型。结果：Ｅ６ 对ＮａＣＮ加缺糖损伤的ＰＣ１２ 细胞保护作用较弱，而对Ｇｌｕ 损伤的原代皮质细胞有较强的保护作用，并降低培养液中一氧化氮（ＮＯ） 的含量。ＮＯ合成前体Ｌ精氨酸（ Ｌａｒｇｉｎｉｎｅ，ＬＡｒｇ）可减弱Ｅ６ 的保护作用。Ｅ６ 对硝普钠（ｓｏｄｉｕｍ ｎｉｔｒｏｐｒｕｓｓｉｄｅ，ＳＮＰ） 损伤的原代神经细胞无保护作用。结论：Ｅ６ 可能是作用于Ｇｌｕ 引起神经元损伤途径中ＮＯ生成之前的环节，从而表现出对缺血样损伤神经细胞的保护作用。
Objective: To observe the protective effect of bisbenzyl isoquinoline compound E6 with strong antagonist activity on ischemic neuronal injury. Methods: Adopting NaCN plus glucose deprivation to induce injury of PC12 cell line and glutamate (Glu) induced cerebral cortical neuron injury in rats. Results: E6 had a weak protective effect on NaCN plus glucose-depleted PC12 cells, but had a protective effect on Glu-damaged primary cortical cells and decreased nitric oxide (NO) content in culture media. NO synthetic precursor L arginine (L arginine, L Arg) can weaken the protective effect of E6. E6 has no protective effect on primary neurons damaged by sodium nitroprusside (SNP). CONCLUSION: E6 may play a role in the pre-NO production of neuronal damage caused by Glu, which may exert a protective effect on ischemia-like injured neurons.