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目的以往体内实验研究表明,乙醇能够引起纹状体、伏隔核和大脑皮层等部位抗坏血酸(AA)的释放,一些药物参与调节乙醇引起的AA的释放。此文要验证原花青素对神经元的直接作用,为乙醇损伤的脑保护治疗提供理论依据。方法原代培养大鼠皮层神经元与AA孵育1～3h后洗去,单独给予乙醇或药物和乙醇共同作用30min,收集细胞外液处理后以HPLC-EC检测抗坏血酸和脱氢抗坏血酸含量。结果原花青素能够抑制乙醇引起的神经元AA释放。谷氨酸能够协同乙醇引起的AA释放,NMDA受体拮抗剂MK-801能够抑制乙醇引起的AA释放,并且低于基础释放水平。结论乙醇可能通过与谷氨酸有关的氧化机制影响神经细胞AA的释放,原花青素参与调节乙醇引起的AA释放作用。
Purpose Previous in vivo experimental studies have shown that ethanol can cause the release of ascorbic acid (AA) in the striatum, nucleus accumbens, and cerebral cortex. Some drugs are involved in the regulation of alcohol-induced AA release. This article to verify the direct effect of proanthocyanidins on neurons, provide a theoretical basis for the protection of ethanol brain injury treatment. Methods Primary cultured rat cortical neurons were incubated with AA for 1 ~ 3 hours and then washed away. Ethanol alone or drug and ethanol were given together for 30 minutes. The contents of ascorbic acid and dehydroascorbic acid were detected by HPLC-EC after the extracellular fluid was collected. Results Proanthocyanidins inhibited ethanol-induced neuronal AA release. Glutamate synergized with ethanol-induced AA release, and the NMDA receptor antagonist MK-801 was able to inhibit ethanol-induced AA release and was below the basal release level. Conclusion Ethanol may affect the release of AA through the oxidation mechanism of glutamate. Proanthocyanidin is involved in the regulation of ethanol-induced AA release.