Department of Forensic Medicine, School of Basic Medical Sciences, Zhengzhou University, Zhengzhou 450001, China.
Alcohol Alcohol. 2020 Jun 25;55(4):357-366. doi: 10.1093/alcalc/agaa031.
Ethanol is a small molecule capable of interacting with numerous targets in the brain, the mechanisms of which are complex and still poorly understood. Studies have revealed that ethanol-induced hippocampal neuronal injury is associated with oxidative stress. Grape seed procyanidin (GSP) is a new type of antioxidant that is believed to scavenge free radicals and be anti-inflammatory. This study evaluated the ability and mechanism by which the GSP improves ethanol-induced hippocampal neuronal injury.
Primary cultures of hippocampal neurons were exposed to ethanol (11, 33 and 66 mM, 1, 4, 8, 12 and 24 h) and the neuroprotective effects of GSP were assessed by evaluating the activity of superoxide dismutase (SOD), the levels of malondialdehyde (MDA) and lactate dehydrogenase (LDH) and cell morphology.
Our results indicated that GSP prevented ethanol-induced neuronal injury by reducing the levels of MDA and LDH, while increasing the activity of SOD. In addition, GSP increased the number of primary dendrites and total dendritic length per cell.
Together with previous findings, these results lend further support to the significance of developing GSP as a therapeutic tool for use in the treatment of alcohol use disorders.
乙醇是一种能够与大脑中众多靶标相互作用的小分子,其机制复杂且仍未被充分理解。研究表明,乙醇诱导的海马神经元损伤与氧化应激有关。葡萄籽原花青素(GSP)是一种新型抗氧化剂,被认为可以清除自由基和抗炎。本研究评估了 GSP 改善乙醇诱导的海马神经元损伤的能力和机制。
原代海马神经元培养物暴露于乙醇(11、33 和 66mM,1、4、8、12 和 24h),通过评估超氧化物歧化酶(SOD)活性、丙二醛(MDA)和乳酸脱氢酶(LDH)水平以及细胞形态来评估 GSP 的神经保护作用。
我们的结果表明,GSP 通过降低 MDA 和 LDH 的水平,同时增加 SOD 的活性,来预防乙醇诱导的神经元损伤。此外,GSP 增加了初级树突的数量和每个细胞的总树突长度。
这些结果与之前的研究结果一起,进一步支持了将 GSP 开发为治疗酒精使用障碍的治疗工具的重要性。