Abstract Context: Oxidative imbalance-induced cognitive impairment is among the most urgent clinical concerns. Isoflurane has been demonstrated to impair cognitive function via an increase in oxidative stress. GSP has strong antioxidant capacities, suggesting potential cognitive benefits. Objective: This study investigates whether GSP pre-treatment can alleviate isoflurane-induced cognitive dysfunction in mice. Materials and methods: C57BL/6J mice were pre-treated with either GSP 25–100 mg/kg/d for seven days or GSP 100–400 mg/kg as a single dose before the 6 h isoflurane anaesthesia. Cognitive functioning was examined using the fear conditioning tests. The levels of SOD, p-NR2B and p-CREB in the hippocampus were also analysed. Results: Pre-treatment with either a dose of GSP 50 mg/kg/d for seven days or a single dose of GSP 200 mg/kg significantly increased the % freezing time in contextual tests on the 1st (72.18 ± 12.39% vs. 37.60 ± 8.93%; 78.27 ± 8.46% vs. 52.72 ± 2.64%), 3rd (93.80 ± 7.62% vs. 52.94 ± 14.10%; 87.65 ± 10.86% vs. 52.89 ± 1.73%) and 7th (91.36 ± 5.31% vs. 64.09 ± 14.46%; 93.78 ± 3.92% vs. 79.17 ± 1.79%) day after anaesthesia. In the hippocampus of mice exposed to isoflurane, GSP 200 mg/kg increased the total SOD activity on the 1st and 3rd day and reversed the decreased activity of the NR2B/CREB pathway. Discussion and conclusions: These findings suggest that GSP improves isoflurane-induced cognitive dysfunction by protecting against perturbing antioxidant enzyme activities and NR2B/CREB pathway. Therefore, GSP may possess a potential prophylactic role in isoflurane-induced and other oxidative stress-related cognitive decline.

中文翻译：

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葡萄籽原花青素对异氟醚致小鼠认知障碍的保护作用

摘要背景：氧化失衡引起的认知障碍是最紧迫的临床问题之一。异氟醚已被证明通过增加氧化应激来损害认知功能。GSP 具有很强的抗氧化能力，表明潜在的认知益处。目的：本研究调查 GSP 预处理是否可以减轻异氟醚诱导的小鼠认知功能障碍。材料和方法：C57BL/6J 小鼠在异氟醚麻醉 6 小时前用 GSP 25–100 mg/kg/d 预处理 7 天或 GSP 100–400 mg/kg 作为单剂量。使用恐惧条件反射测试检查认知功能。还分析了海马中 SOD、p-NR2B 和 p-CREB ​​的水平。结果：用 7 天的 GSP 50 mg/kg/d 剂量或单剂量的 GSP 200 mg/kg 预处理显着增加了第一天上下文测试中的冻结时间百分比（72.18 ± 12.39% 与 37.60 ± 8.93 %; 78.27 ± 8.46% vs. 52.72 ± 2.64%), 第三名 (93.80 ± 7.62% vs. 52.94 ± 14.10%; 87.65 ± 10.86% vs. 52.89 ± 1.76% vs. 4.73% 4 ±4.5%) %; 93.78 ± 3.92% vs. 79.17 ± 1.79%) 麻醉后一天。在暴露于异氟醚的小鼠海马体中，GSP 200 mg/kg 增加了第 1 天和第 3 天的总 SOD 活性，并逆转了 NR2B/CREB ​​通路活性的降低。讨论和结论：这些发现表明 GSP 通过防止干扰抗氧化酶活性和 NR2B/CREB ​​通路来改善异氟醚诱导的认知功能障碍。所以，