【摘要】 长期大量饮酒会导致慢性乙醇中毒，造成神经系统发生严重损害，出现焦虑、记忆力减退等症状。研究表明，神经细胞凋亡是乙醇诱导神经系统损伤的重要机制之一。慢性乙醇暴露可导致神经细胞内N-甲基-D-天冬氨酸受体处于兴奋状态，也可使得肌醇1,4,5-三磷酸受体1和肌浆/内质网Ca²⁺-ATP酶表达增强，钙离子电压门控通道功能增强，导致Ca²⁺大量进入细胞，产生钙超载，激活细胞内钙蛋白酶、caspase等依赖性激酶与钙调蛋白，诱导神经元变性和凋亡，从而导致神经系统疾病。细胞内钙超载还会导致线粒体、内质网的损伤，最终导致细胞凋亡。本文对慢性乙醇暴露通过钙超载诱导神经细胞凋亡进而引发神经系统疾病的机制展开系统综述，以期为酒精使用障碍和慢性酒精中毒性脑病等神经系统疾病完善其病因学基础，并寻找可能的治疗靶点。更多还原

【Abstract】 Long-term heavy drinking can lead to chronic alcohol poisoning, causing serious damage to the nervous system, including anxiety, memory loss and other symptoms. Studies have shown that apoptosis of neurons is one of the important mechanisms of ethanol-induced nervous system damage. Chronic ethanol exposure can lead to the excitability of N-methyl-D-aspartate receptor in neurons, increase the expression of inositol 1,4,5-triphosphate receptor 1 and sarco/endoplasmic reticulum Ca²⁺-ATPase, and enhance the function of calcium ion voltage-gated channels, resulting in a large amount of Ca²⁺ entering cells. Calcium overload activates intracellular calpain, caspase and other dependent kinases and calmodulin, inducing neuronal degeneration and apoptosis, leading to neurological diseases. Intracellular calcium overload can also cause damage to mitochondria and endoplasmic reticulum, and eventually lead to apoptosis. In this study, we systematically review the mechanism of chronic alcohol exposure-induced neuronal apoptosis and neurological diseases through calcium overload, in order to improve the etiological basis for alcohol use disorder, chronic alcoholic encephalopathy and other neurological diseases, aiming to find potential therapeutic targets.更多还原