摘要
目的:探讨红景天苷(Sal)对血管性痴呆(VD)大鼠认知功能障碍的治疗作用,并从抑制氧化应激、改善线粒体功能等方面研究其可能机制。方法:选用57只健康雄性SD大鼠随机等分为假手术组(sham)、双侧颈总动脉结扎组(2-VO)和红景天苷治疗组(Sal),采用双侧颈总动脉结扎法复制2-VO模型。采用Morris水迷宫实验检测各组大鼠的学习、记忆等认知功能。700B放大器记录海马长时程增强(LTP)。利用试剂盒检测超氧化物歧化酶(SOD)、谷胱甘肽过氧化物酶(GSH-Px)、谷胱甘肽(GSH)、丙二醛(MDA)等指标,评估海马氧化应激水平。检测海马线粒体膜电位、腺嘌呤核苷三磷酸(ATP)等,评估线粒体功能。结果:2-VO组大鼠逃避潜伏期较sham组显著延长,原目标象限停留时间较假手术组显著缩短(P <0.05,n=8),Sal组较2-VO组逃避潜伏期缩短、原目标象限停留时间延长(P <0.05,n=8);2-VO组较sham组CA1区f EPSP增强幅度显著减弱(P <0.05,n=6),Sal组f EPSP增强幅度较2-VO组显著提高(P <0.05,n=6);与sham组相比,2-VO组大鼠海马组织SOD、GSH-Px、GSH显著降低(P <0.05),MDA显著增高(P <0.05,n=8)。Sal组SOD、GSH-Px、GSH较2-VO组显著升高(P <0.05,n=8),MDA较2-VO组显著降低(P <0.05,n=8);2-VO组大鼠海马区线粒体膜电位、ATP水平均较sham组显著下降(P <0.05,n=8),Sal组膜电位、ATP水平较2-VO组显著升高(P <0.05,n=8)。结论:Sal可显著改善2-VO大鼠认知功能障碍,提高海马区LTP水平,其机制可能和抑制2-VO大鼠海马区的氧化应激水平并改善其线粒体功能有关。
Objective: To investigate the therapeutic effect of Salidroside on cognitive dysfunction in rats with vascular dementia (2-VO),and to explore its possible mechanism about inhibiting oxidative stress and improving mitochondrial function. Methods: Fifty-seven male Sprague-Dawley rats were randomly divided into three groups: sham group,model group,and salidroside group. The 2-VO model was established by bilateral general cervical artery ligation. The learning and memory ability was detected by Morris water maze test. Hippocampal long-term potentiation (LTP) was measured using 700 B amplifier in rat brain slices. Superoxide dismutase (SOD),glutathione peroxidase (GSH-Px),Glutathione (GSH) and maleic dialdehyde (MDA) in the hippocampal homogenate were measured;The mitochondrial membrane potential and ATP in the hippocampus were detected. Results: Compared with sham group,the escape latency was prolonged,and the swimming time in the target quadrant was decreased in the Model group (P < 0. 05).Salidroside could significantly reverse the changes (P < 0. 05). Salidroside could attenuate inhibition of hippocampal LTP in 2-VO rats (P < 0. 05). Chronic ischemia could significantly increase content of MDA,decrease content of GSH and decreased the activities of SOD and GSH-PX in the homogenate of hippocampus (P < 0. 05),which could be reversed by salidroside (P < 0. 05). Salidroside could attenuate the drops of the mitochondrial membrane potential and ATP in the hippocampus in 2-VO rats (P < 0. 05). Conclusion: Salidroside could significantly improve cognitive dysfunction and the hippocampal LTP in 2-VO rats. The mechanism may be related to the inhibition of oxidative stress and the improvement of mitochondrial function in hippocampus.
作者
吕文海
郑涛
Lv Wenhai;Zheng Tao(Department of Neurosurgery,Xi'an Fengcheng Hospital,Xi'an 710000;Department of Neurosurgery,Xi'an International Medical Center Hospital,Xi'an 710100,China)
出处
《神经解剖学杂志》
CSCD
2021年第4期443-448,共6页
Chinese Journal of Neuroanatomy
关键词
红景天苷
血管性痴呆
氧化应激
线粒体功能
大鼠
salidroside
vascular dementia
oxidative stress
mitochondrial function
rat
