HONG Chen, HU Wenjun, WANG Shuna, LI Zhiyong, MIAO Chaoyu. Establishment and evaluation of in vivo and in vitro D-galactose induced cognitive impairment models[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 14-18,73. doi: 10.3969/j.issn.1006-0111.2019.01.004
| Citation:
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HONG Chen, HU Wenjun, WANG Shuna, LI Zhiyong, MIAO Chaoyu. Establishment and evaluation of in vivo and in vitro D-galactose induced cognitive impairment models[J]. Journal of Pharmaceutical Practice and Service, 2019, 37(1): 14-18,73. doi: 10.3969/j.issn.1006-0111.2019.01.004
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Establishment and evaluation of in vivo and in vitro D-galactose induced cognitive impairment models
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Department of Pharmacology, School of Pharmacy, Naval Medical University, Shanghai 200433, China
- Received Date: 2018-07-02
- Rev Recd Date:
2018-09-12
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Abstract
Objective To construct and explore the in vivo and in vitro D-galactose induced cognitive impairment models and evaluate the application value of the combined models in the study of cognitive impairments. Methods The cognitive impairment mice model induced by D-gal was prepared by continuous intraperitoneal injection of D-gal saline solution for 8 weeks, followed by detection of learning and memory functions with Morris water maze. The related molecular markers in the brain tissue were assayed to evaluate the effect and application value. D-gal cell model was prepared by adding D-gal in different concentrations into the cell cultural medium of neurons harvested from the hippocampus of young mice. The effect and application value were evaluated by detecting the molecular markers related to the level of cell injury. Results The Morris water maze on the D-gal model showed that the learning and memory functions of mice in the model group were significantly lower than those in the control group. Meanwhile, the levels of apoptosis and oxidative stress in the model group were significantly higher than those in the control group. In the hippocampal neuron model of D-gal, the neurons showed a dose-dependent morphologic and functional change with the increase of D-gal dose and the levels of apoptosis and oxidative stress were significantly higher than those in the negative control. Conclusion D-galactose can be successfully used to induce cognitive impairment models both in vivo and in vitro through the decrease of the learning and memory functions of mice and induction of apoptosis and oxidative stress in neurons. Combined application of the two models of D-gal can be one of effective and promising tools for the study of cognitive impairment and pharmacodynamic evaluation.
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