摘要
Objective: To observe the effect of electroacupuncture(EA) on cytochrome c oxidase(COX) activity of hippocampal mitochondria in senescence-accelerated mouse prone 8(SAMP8) mice, and to explore the EA mechanism on Alzheimer disease(AD) in improving energy metabolic disorder. Methods: Twelve SAMP8 mice were randomly divided into a model group and an EA group, with six in each group. Six senescence-accelerated mouse resistance 1(SAMR1) mice were prepared as blank group. Mice in the EA group received EA on Baihui(GV 20) and Yongquan(KI 1), once a day for 7 d as a course, altogether 3 courses with one day interval between two courses. Mice in the model group and the blank group were manipulated and fixed as those in the EA group. After interventions, Morris water maze was employed to test spatial learning and memory ability to evaluate EA effect; spectrophotometry was used to detect the activity of hippocampal mitochondria COX. Results: Compared with the blank group, mean escape latencies of the EA group and model group were prolonged significantly in Morris water maze tests(P<0.01), the residue duration in the former platform quadrant significantly decreased(P<0.01). Compared with the model group, mean escape latencies on 1 d, 2 d and 3 d of the EA group were significantly reduced(P<0.05), and those on 4 d and 5 d continued the decreasing tendency(P<0.01), the residue duration on the former platform quadrant was significantly prolonged(P<0.05). The COX activity tests showed that, compared with the blank group, COX activities of the model group and the EA group were significantly decreased(P<0.01); compared with the model group, COX activity of the EA group was significantly elevated(P<0.01). Conclusion: It's plausible that EA improves AD learning and memory ability by increasing mitochondria COX activity, protecting the structure and function, and improving energy metabolism.
Objective： To observe the effect of electroacupuncture （EA） on cytochrome c oxidase （COX）activity of hippocampal mitochondria in senescence-accelerated mouse prone 8 （SAMP8） mice, and to explore the EA mechanism on Alzheimer disease （AD） in improving energy metabolic disorder. Methods： Twelve SAMP8 mice were randomly divided into a model group and an EA group, with six in each group. Six senescence-accelerated mouse resistance 1 （SAMR1） mice were prepared as blank group. Mice in the EA group received EA on Baihui （GV 20） and Yongquan （KI 1）, once a day for 7 d as a course, altogether 3 courses with one day intervalbetween two courses. Mice in the model group and the blank group were manipulated and fixed as those in the EA group. After interventions, Morris water maze was employed to test spatial learning and memory ability to evaluate EA effect; spectrophotometry was used to detect the activity of hippocampal mitochondria COX. Results： Compared with the blank group, mean escape latenciesof the EA group and model group were prolonged significantly in Morris water maze tests （P〈0.01）, the residue duration in the former platform quadrant significantly decreased （P〈0.01）. Compared with the model group, mean escape latencies on 1 d, 2 d and 3 d of the EA group were significantly reduced （P〈0.05）, and those on 4 d and 5 d continued the decreasing tendency （P〈0.01）, the residue duration on the former platform quadrant was significantly prolonged （P〈0.05）. The COX activity tests showed that, compared with the blank group, COX activities of the model group and the EA group were significantly decreased （P〈0.01）; compared with the model group, COX activity of the EA group was significantly elevated （P〈0.01）. Conclusion： It＇s plausible that EA improves AD learning and memory ability by increasing mitochondria COX activity, protecting the structure and function, and improving energy metabolism.
基金
supported by National Natural Science Foundation of China (No.30472235)
Scientific Science Foundation for the Youth of the Education Department of Sichuan Province (No. 2006B023)
