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葡萄粉可预防创伤后应激障碍大鼠模型的认知、行为和生化损伤。

Grape powder prevents cognitive, behavioral, and biochemical impairments in a rat model of posttraumatic stress disorder.

机构信息

Department of Pharmacological and Pharmaceutical Sciences, University of Houston, TX, USA.

Department of Pharmacological and Pharmaceutical Sciences, University of Houston, TX, USA.

出版信息

Nutr Res. 2015 Jan;35(1):65-75. doi: 10.1016/j.nutres.2014.11.008. Epub 2014 Dec 5.

Abstract

Previously, using the single-prolonged stress (SPS) rat model of posttraumatic stress disorder, we reported that moderate treadmill exercise, via modulation of oxidative stress-related mechanisms, rescued anxiety- and depression-like behaviors and reversed SPS-induced memory impairment. In this study using the SPS model (2-hour restrain, 20-minute forced swimming, 15-minute rest, and 1-2-minute diethyl ether exposure), we hypothesized that antioxidant rich grape powder (GP) prevents SPS-induced behavioral and memory impairment in rats. Male Sprague Dawley rats were randomly assigned into control (CON) (provided tap water), SPS (provided tap water), GP-SPS (provided 15 g/L GP in tap water for 3 weeks followed by SPS), or GP-CON (3 weeks of GP followed by CON exposure). Anxiety- and depression-like behaviors were significantly greater in SPS rats, when compared with CON- or GP-treated rats, and GP reversed these behavioral deficits. Single-prolonged stress rats made significantly more errors in both short- and long-term memory tests compared with CON- or GP-treated rats, which were prevented in GP-SPS rats. Grape powder prevented SPS-induced increase in plasma corticosterone level. Furthermore, brain-derived neurotrophic factor levels were significantly decreased in amygdala of SPS rats but not in GP-SPS rats compared with CON or (GP-CON) rats. In addition, GP significantly increased acetylated histone 3 and histone deacetylase 5 in hippocampus and amygdala of SPS rats as compared with CON or GP-CON rats. In conclusion, we suggest protective role of GP in SPS-induced behavioral, cognitive, and biochemical impairments in rats. Perhaps, epigenetic regulation of brain-derived neurotrophic factor enables GP-mediated prevention of SPS-induced deficits in rats.

摘要

先前,我们使用创伤后应激障碍的单一延长压力(SPS)大鼠模型报告说,适度的跑步机运动通过调节氧化应激相关机制,挽救了焦虑和抑郁样行为,并逆转了 SPS 引起的记忆障碍。在本研究中,我们使用 SPS 模型(2 小时限制,20 分钟强制游泳,15 分钟休息和 1-2 分钟二乙醚暴露),假设富含抗氧化剂的葡萄粉(GP)可预防 SPS 诱导的大鼠行为和记忆障碍。雄性 Sprague Dawley 大鼠被随机分为对照组(CON)(提供自来水),SPS(提供自来水),GP-SPS(提供自来水 15g/L GP 持续 3 周,然后 SPS)或 GP-CON(3 周 GP 后再暴露于 CON)。与 CON 或 GP 处理的大鼠相比,SPS 大鼠的焦虑和抑郁样行为明显增加,而 GP 则逆转了这些行为缺陷。与 CON 或 GP 处理的大鼠相比,SPS 大鼠在短期和长期记忆测试中均犯了更多的错误,而 GP-SPS 大鼠则避免了这种情况。葡萄粉可防止 SPS 引起的血浆皮质酮水平升高。此外,与 CON 或(GP-CON)大鼠相比,SPS 大鼠杏仁核中的脑源性神经营养因子水平显着降低,但在 GP-SPS 大鼠中则没有。此外,与 CON 或 GP-CON 大鼠相比,GP 显着增加了 SPS 大鼠海马体和杏仁核中的乙酰化组蛋白 3 和组蛋白去乙酰化酶 5。总之,我们建议 GP 在 SPS 诱导的大鼠行为,认知和生化损伤中起保护作用。也许,脑源性神经营养因子的表观遗传调节使 GP 能够预防 SPS 诱导的大鼠缺陷。

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