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Effect of Kangshuai Yizhi Formula I (抗衰益智方 I) on learning and memory dysfunction induced by scopolamine in mice
- Chinese Journal of Integrative Medicine Vol. 16, Issue 3, Pages: 252-257(2010)
- Affiliations：
Department of Pathophysiology, Medical School of Jinan University,Guangzhou,China
- Author bio：
- Funds：Supported by Special Fund for Doctor Discipline Research of Ministry of Education (No. 20060559003), Key Programs for Science and Technology Development of Guangzhou (2008J1-C181)
DOI：10.1007/s11655-010-0252-3
CLC：Published：2010，
Published Online：8 August 2010，
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Wei, J., Lu, Dx., Qi, Rb. et al. Effect of Kangshuai Yizhi Formula I (抗衰益智方 I) on learning and memory dysfunction induced by scopolamine in mice., Chin. J. Integr. Med. 16, 252–257 (2010). https://doi.org/10.1007/s11655-010-0252-3
Jia Wei, Da-xiang Lu, Ren-bin Qi, et al. Effect of Kangshuai Yizhi Formula I (抗衰益智方 I) on learning and memory dysfunction induced by scopolamine in mice. [J]. Chinese Journal of Integrative Medicine 16(3):252-257(2010)
Wei, J., Lu, Dx., Qi, Rb. et al. Effect of Kangshuai Yizhi Formula I (抗衰益智方 I) on learning and memory dysfunction induced by scopolamine in mice., Chin. J. Integr. Med. 16, 252–257 (2010). https://doi.org/10.1007/s11655-010-0252-3 DOI：
Jia Wei, Da-xiang Lu, Ren-bin Qi, et al. Effect of Kangshuai Yizhi Formula I (抗衰益智方 I) on learning and memory dysfunction induced by scopolamine in mice. [J]. Chinese Journal of Integrative Medicine 16(3):252-257(2010) DOI： 10.1007/s11655-010-0252-3.
摘要
To evaluate the improvement of Kangshuai Yizhi Formula I (抗衰益智方 I
KYF I) on: the learning and memory dysfunction in mice
and on the mechanism of the hippocampal cholinergic system and the nervous system of monoamine which are closely related to learning and memory function. Mice: in the low-
middle-
and high-dose KYF I groups were given low-
middle-
and high-dose KYF
respectively
by gastrogavage for 35 successive days. Animals in the control group and the model group were treated with distilled water. The acute learning and memory dysfunction model was established by injection of scopolamine from day 31
and Morris water maze was used to assess the behavior performance of scopolamine-induced model mice for five days. The activities of acetylcholinesterase (AChE)
choline acetyl transferase (ChaT) and the content of monoamine neurotransmitters in hippocampus were measured. The activity of monoamine oxidase (MAO) in hippocampus and serum was also detected. (1) Compared with the control group
the: mean escape latency was shortened
and the frequency across the platform and the staying time at the platform area on the 5th day were decreased in the model group by Morris water maze test. The activities of AChE and MAO were increased
and the ChaT activity and monoamine neurotransmitter content were decreased as well. (2) The escape latency for 4 days in the low-
middle-
and high-dose KYF I groups was significantly shortened than that in the model group
with the shortest latency in the high-dose KYF I group (P<0.05
P<0.01). The frequency across the platform was significantly increased and the staying time at the platform was significantly prolonged in the middle- and high-dose KYF I groups (P<0.05
P<0.01). (3) As compared with the model group
the activity of ChaT and the content of monoamine neurotransmitters in the hippocampus were significantly increased
and the activities of AchE and MAO were significantly decreased in the hippocampus in the high-dose KYF I group (P<0.01). High-dose KYF I can significantly improve the learning and memory dysfunction: induced by scopolamine in mice. Its mechanism may be related to improving the central cholinergic system and regulating the hippocampal monoamine neurotransmitters.
Abstract
To evaluate the improvement of Kangshuai Yizhi Formula I (抗衰益智方 I
KYF I) on: the learning and memory dysfunction in mice
and on the mechanism of the hippocampal cholinergic system and the nervous system of monoamine which are closely related to learning and memory function. Mice: in the low-
middle-
and high-dose KYF I groups were given low-
middle-
and high-dose KYF
respectively
by gastrogavage for 35 successive days. Animals in the control group and the model group were treated with distilled water. The acute learning and memory dysfunction model was established by injection of scopolamine from day 31
and Morris water maze was used to assess the behavior performance of scopolamine-induced model mice for five days. The activities of acetylcholinesterase (AChE)
choline acetyl transferase (ChaT) and the content of monoamine neurotransmitters in hippocampus were measured. The activity of monoamine oxidase (MAO) in hippocampus and serum was also detected. (1) Compared with the control group
the: mean escape latency was shortened
and the frequency across the platform and the staying time at the platform area on the 5th day were decreased in the model group by Morris water maze test. The activities of AChE and MAO were increased
and the ChaT activity and monoamine neurotransmitter content were decreased as well. (2) The escape latency for 4 days in the low-
middle-
and high-dose KYF I groups was significantly shortened than that in the model group
with the shortest latency in the high-dose KYF I group (P<0.05
P<0.01). The frequency across the platform was significantly increased and the staying time at the platform was significantly prolonged in the middle- and high-dose KYF I groups (P<0.05
P<0.01). (3) As compared with the model group
the activity of ChaT and the content of monoamine neurotransmitters in the hippocampus were significantly increased
and the activities of AchE and MAO were significantly decreased in the hippocampus in the high-dose KYF I group (P<0.01). High-dose KYF I can significantly improve the learning and memory dysfunction: induced by scopolamine in mice. Its mechanism may be related to improving the central cholinergic system and regulating the hippocampal monoamine neurotransmitters.
关键词
dysmnesiccholinergicmonoamine neurotransmittersmonoamine oxidase
Keywords
dysmnesiccholinergicmonoamine neurotransmittersmonoamine oxidase
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