Department of Pharmacological and Pharmaceutical Sciences, University of Houston, TX, USA.
Department of Pharmacological and Pharmaceutical Sciences, University of Houston, TX, USA.
Nutr Res. 2015 Jan;35(1):65-75. doi: 10.1016/j.nutres.2014.11.008. Epub 2014 Dec 5.
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.
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。