Apple polyphenols (AP) have attracted much attention due to their various bioactivities. In this study, the protective effect of AP against chronic ethanol exposure-induced neural injury as well as the possible mechanisms were investigated. Body weight, daily average food intake and daily average fluid intake were measured and daily average ethanol consumption was calculated. The influences of AP on motor behavior and memory were detected by locomotor activity test, rotarod test, beam walking test, and Y maze test and novel object recognition test, respectively. The changes of blood ethanol concentration and the oxidative stress were also measured. AP improved chronic ethanol exposure-induced the inhibition of body weight and the decrease of daily average food intake, but did not influence the daily average fluid intake and the daily average ethanol intake, indicating that the improve effect of AP did not result from the decrease of ethanol intake. Motor activity and motor coordination were not influenced after chronic ethanol exposure though the blood ethanol concentration was higher than that in control group. AP improved significantly chronic ethanol ethanol-induced the memory impairment and the hippocampal CA1 neurons damage. Further studies found that AP decreased the contents of NO and MDA and increased the levels of T-AOC and GSH in the hippocampus of rats. These results suggest that AP exerts a protective effect against chronic ethanol induced memory impairment through improving the oxidative stress in the hippocampus.

中文翻译：

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苹果多酚对慢性乙醇暴露引起的大鼠神经损伤的保护作用。

苹果多酚（AP）由于其多种生物活性而备受关注。在这项研究中，研究了AP对慢性乙醇暴露引起的神经损伤的保护作用及其可能的机制。测量体重，每日平均食物摄入量和每日平均液体摄入量，并计算每日平均乙醇消耗量。分别通过运动能力测试，旋转脚架测试，横梁行走测试，Y迷宫测试和新型物体识别测试来检测AP对运动行为和记忆的影响。还测量了血液中乙醇浓度和氧化应激的变化。AP改善了慢性乙醇暴露引起的体重抑制和每日平均食物摄入量的减少，但不影响每日平均体液摄入量和每日平均乙醇摄入量，表明AP的改善效果并非源于乙醇摄入量的减少。尽管血液中的乙醇浓度高于对照组，但长期暴露于乙醇后，对运动活动和运动协调性没有影响。AP显着改善了慢性乙醇乙醇引起的记忆障碍和海马CA1神经元损伤。进一步的研究发现，AP降低了大鼠海马中NO和MDA的含量，并增加了T-AOC和GSH的水平。这些结果表明，AP通过改善海马中的氧化应激而对慢性乙醇诱导的记忆障碍具有保护作用。提示AP的改善效果并非来自乙醇摄入量的减少。慢性乙醇暴露后，虽然血液中的乙醇浓度高于对照组，但运动能力和运动协调性并未受到影响。AP显着改善了慢性乙醇乙醇引起的记忆障碍和海马CA1神经元损伤。进一步的研究发现，AP降低了大鼠海马中NO和MDA的含量，并增加了T-AOC和GSH的水平。这些结果表明，AP通过改善海马中的氧化应激而对慢性乙醇诱导的记忆障碍具有保护作用。提示AP的改善效果并非来自乙醇摄入量的减少。慢性乙醇暴露后，虽然血液中的乙醇浓度高于对照组，但运动能力和运动协调性并未受到影响。AP明显改善了慢性乙醇乙醇引起的记忆障碍和海马CA1神经元损伤。进一步的研究发现，AP降低了大鼠海马中NO和MDA的含量，并增加了T-AOC和GSH的水平。这些结果表明，AP通过改善海马中的氧化应激而对慢性乙醇诱导的记忆障碍具有保护作用。慢性乙醇暴露后，虽然血液中的乙醇浓度高于对照组，但运动能力和运动协调性并未受到影响。AP显着改善了慢性乙醇乙醇引起的记忆障碍和海马CA1神经元损伤。进一步的研究发现，AP降低了大鼠海马中NO和MDA的含量，并增加了T-AOC和GSH的水平。这些结果表明，AP通过改善海马中的氧化应激而对慢性乙醇诱导的记忆障碍具有保护作用。慢性乙醇暴露后，虽然血液中的乙醇浓度高于对照组，但运动能力和运动协调性并未受到影响。AP明显改善了慢性乙醇乙醇引起的记忆障碍和海马CA1神经元损伤。进一步的研究发现，AP降低了大鼠海马中NO和MDA的含量，并增加了T-AOC和GSH的水平。这些结果表明，AP通过改善海马中的氧化应激而对慢性乙醇诱导的记忆障碍具有保护作用。