Zhen ci yan jiu = Acupuncture research · 2015
[Effect of electroacupuncture stimulation of "Baihui" (GV 20) and " Yongquan" (KI 1) on expression of hippocampal amyloid-β and low density lipoprotein receptor-related protein-1 in APP/PS 1 transgenic mice].
Аннотация на английскомСтатьяПоддержка исследования: вне правительства СШАНазвание и аннотация: Перевод пока не подготовлен
Обработка статьи · этапы, ошибки и управление
Загрузка состояния…
Ошибки и ограничения
История · было → стало
Состояние обновляется каждые 5 секунд, пока блок открыт. Процент показывается только там, где известен объём работы. Пауза останавливает продолжение этапа; текущий запрос к источнику может завершиться.
Li Fu, Li Li-na, Wang Xin, Bai Yang, Jiawula Abulizi, Bu Qing-yun, Gao Tang-ke, Xue Wei-guo
Аннотация
OBJECTIVE: To observe the effect of electroacupuncture (EA) treatment on the level of hippocampal amyloid-beta peptide (Aβ) and its key transport receptor low density lipoprotein receptor-related protein-1 (LRP 1) in APP/PS 1 transgenic mice so as to explore its mechanism underlying improvement of Alzheimer's disease (AD).
METHODS: Twenty-four male APP/PS 1 transgenic mice were equally and randomly divided into model group and EA treatment group, and 12 C 57 BL/6 mice were used as the normal control group. EA (1 Hz/50 Hz, 0.3 mA) was applied to "Baihui" (GV 20) and "Yongquan" (KI 1) for 15 min, once every other day for 6 weeks. The learning-memory ability was detected by using Morris water maze testing, left hippocampal Aβ 1-40 and Aβ 1-42 contents were assayed by ELISA, and right hippocampal LRP 1 expression was detected using Western blot (WB).
RESULTS: Results of Morris water maze test showed no significant differences among the three groups in the escape latency, the times of the platform-site crossovers, the time spent in the target platform quadrant (P>0.05). Compared with the model group, the moderately increased escape latency had a decreasing tendency in the EA treatment group. ELISA assaying showed that hippocampal Aβ 1-42, Aβ 1-40, and ratio of Aβ 1-42/Aβ 1-40 of the model group were significantly higher than those of the normal control group (P<0.01). After EA intervention, the increased Aβ 1-42 , Aβ 1-40, and ratio of Aβ 1-42/Aβ 1-40 were remarkably down-regulated in the EA treatment group (P<0.01). WB detection displayed that the right hippocampal LRP 1 expression level of the model group was markedly lower than that of the normal control group (P<0.05). After EA treatment, LRP 1 expression level was moderately up-regulated but without significant difference between the model and EA treatment groups (P>0.05).
CONCLUSION: EA intervention can lower the level of hippocampal Aβ in APP/PS 1 transgenic mice, but its effects on Aβ transport receptor LRP 1 expression and learning-memory ability need being confirmed further.
METHODS: Twenty-four male APP/PS 1 transgenic mice were equally and randomly divided into model group and EA treatment group, and 12 C 57 BL/6 mice were used as the normal control group. EA (1 Hz/50 Hz, 0.3 mA) was applied to "Baihui" (GV 20) and "Yongquan" (KI 1) for 15 min, once every other day for 6 weeks. The learning-memory ability was detected by using Morris water maze testing, left hippocampal Aβ 1-40 and Aβ 1-42 contents were assayed by ELISA, and right hippocampal LRP 1 expression was detected using Western blot (WB).
RESULTS: Results of Morris water maze test showed no significant differences among the three groups in the escape latency, the times of the platform-site crossovers, the time spent in the target platform quadrant (P>0.05). Compared with the model group, the moderately increased escape latency had a decreasing tendency in the EA treatment group. ELISA assaying showed that hippocampal Aβ 1-42, Aβ 1-40, and ratio of Aβ 1-42/Aβ 1-40 of the model group were significantly higher than those of the normal control group (P<0.01). After EA intervention, the increased Aβ 1-42 , Aβ 1-40, and ratio of Aβ 1-42/Aβ 1-40 were remarkably down-regulated in the EA treatment group (P<0.01). WB detection displayed that the right hippocampal LRP 1 expression level of the model group was markedly lower than that of the normal control group (P<0.05). After EA treatment, LRP 1 expression level was moderately up-regulated but without significant difference between the model and EA treatment groups (P>0.05).
CONCLUSION: EA intervention can lower the level of hippocampal Aβ in APP/PS 1 transgenic mice, but its effects on Aβ transport receptor LRP 1 expression and learning-memory ability need being confirmed further.