摘要
目的探讨葡萄籽原花青素对睡眠呼吸暂停模式低氧大鼠海马区线粒体损伤及学习记忆的影响。方法80只雄性SD大鼠分成对照组、模型组、高、低剂量萄籽原花青素组。对照组暴露于空气中，模型组暴露于低氧条件下（50ml／L，暴露时间每天8h，持续时间2，6周），电镜观察海马区神经细胞超微结构，比色法检测大脑组织丙二醛（MDA）水平和超氧化物歧化酶（SOD）水平，原位缺口末端标记法（TUNEL）检测凋亡细胞，水迷宫测试动物学习记忆功能。结果与对照组比较，低氧后线粒体结构损伤、MDA含量明显升高[（79．86±2．52）μmol／g，（88．26±2．86）μmol／g]、SOD活性显著降低[（70．67±6．70）μmol／g，（64．26±7．86）μmol／g]、TUNEL阳性细胞增多[（9．68±0．79）个／视野，（15．9±2．92）个／视野]，水迷宫检测动物逃避潜伏期时间延长、穿台次数减少（P〈0．05）；与模型组比较，葡萄籽原花青素低剂量组能减轻线粒体超微结构的损伤，降低MDA含量[（76．38±1．96），（82．16．4-2．02）]、提高SOD活性[（76．20±6．86），（70．58±6．86）]、减少TUNEL阳性细胞[（6．60±0．69），（9．54±1．36）]；水迷宫检测动物逃避潜伏期时间缩短、穿台次数增多（P〈0．05）；与低剂量组比较，高剂量组线粒体超微结构的损伤明显减轻，MDA含量降低、SOD活性增高、TUNEL阳性细胞减少；水迷宫检测动物逃避潜伏期时间缩短、穿台次数增多（P〈0．05）。结论葡萄籽原花青素减轻睡眠呼吸暂停模式低氧大鼠海马区线粒体结构损伤，改善学习记忆功能。
Objective To investigate the effects of grape seed proanthocyanidin（GSPE） on mitochondrial injury in hippocampus and learning-memory impairment after obstructive sleep apnea hypoxia in rats. Methods Male SD rats（n--80） were randomly divided into control group,model group,low dose of GSPE treat- ment group and high dose of GSPE treatment group. Rats in control group were exposed in air, the model group were suffered from intermittent hypoxia conditions （50 ml/L, 8-hour-intermittent hypoxia everyday, and the duration of experiment 2 and 6 weeks, respectively）. Mitochondrion pathology in hippocampal region was observed using elec- tron microscope;malondialdehyde （MDA） contents and superoxide dismutase activity were detected by colorimetry and apoptotic cells was measured by TUNEL method. The cognitive function of rats in each group was assessed with the Morris water maze （MWM）. Results After hypoxia, mitochondrion was significantly injured. The MDA contents were increased（79.86 ±2.52,88.26 ±2.86） and SOD level decreased（70.67 ±6.70,64.26 ±7.86）. The number of neural apoptotic cells was significantly enhanced （9.68 ± 0.79,15.9 ± 2.92 ）. MWM test showed that the escaping latency was prolonged and the frequency of crossing the platform was decreased （ P 〈 0.05 ）. Compared with that in the model group, low dose of GSPE decreased MDA contents （76.38 ：e 1.96,82. 16 ± 2.02 ） ,increased SOD level（ 76.20 ± 6.86,70.58 ± 6.86 ） , and decreased apoptotie cells （ 6.60 ±0.69,9.54 ± 1.36）. MWM test showed that the escaping latency was shortened and the frequency of crossing the platform was increased in GSPE treatment groups（ P 〈 0.05）. Compared with low dose of GSPE,high dose of GSPE decreased MDA decontents increased SOD level and decreased apoptotic cells. MWM test showed that the escaping latency was shortened and the frequency of crossing the platform was increased （ P 〈 0.05 ）. Conclusion GSPE can attenuate mitoehondrial injury and improve learning-memory function after obstructive sleep apnea hypoxia.
出处
《中华行为医学与脑科学杂志》
CAS
CSCD
北大核心
2013年第7期584-586,共3页
Chinese Journal of Behavioral Medicine and Brain Science
基金
河北省教育厅重点资助项目（ZH2012046）
