Autor: |
HUANG Jia, WANG Mengxue, NI Jinglei, LIANG Shengxiang, LIN Bingbing |
Jazyk: |
English<br />Chinese |
Rok vydání: |
2022 |
Předmět: |
|
Zdroj: |
康复学报, Vol 32, Pp 510-517 (2022) |
Druh dokumentu: |
article |
ISSN: |
2096-0328 |
DOI: |
10.3724/SP.J.1329.2022.06006 |
Popis: |
ObjectiveTo analyze the correlation between the changes of learning and memory and the progressive degeneration of white matter nerve fibers and pericytes in the corpus callosum and hippocampus of rats with chronic cerebral ischemia, then to explore the mechanism of learning and memory impairment caused by chronic cerebral ischemia, and provide a possible predictive target for vascular cognitive impairment.MethodsA total of 24 SPF male SD rats were divided randomly into sham operation group, 28 days after operation group and 56 days after operation group, with eight rats in each group. The sham operation group were treated with bilateral common carotid arteries separation without ligation, and chronic cerebral ischemia models were established by ligation of bilateral common carotid arteries in the 28 days after operation group and the 56 days after operation group. At 28 d and 56 d after operation, morris water maze was used to detect spatial learning and memory ability; diffusion tensor imaging was used to observe the fractional anisotropy (FA) and mean diffusivity (MD) rate of white matter nerve fibers in corpus callosum and hippocampus; luxol fast blue (LFB) staining was used to observe demyelination in corpus callosum; Western blot was used to detect the expression of myelin basic protein (MBP) and pericyte marker platelet-derived growth factor receptor β (PDGFR-β) in corpus callosum and hippocampus.Results(1) Learning and memory ability: compared with the sham operation group, the escape latency prolonged significantly from day 2 to day 4 after operation in the 28 days after operation group and on the 3rd day in the 56 days after operation group (PPPr=0.832, Pr=0.777, PPPP |
Databáze: |
Directory of Open Access Journals |
Externí odkaz: |
|