151. Fracture shortly before stroke in mice leads to hippocampus inflammation and long-lasting memory dysfunction.
- Author
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Li Z, Wei M, Lyu H, Huo K, Wang L, Zhang M, and Su H
- Subjects
- Animals, Male, Maze Learning, Mice, Mice, Transgenic, Fractures, Bone complications, Fractures, Bone metabolism, Fractures, Bone pathology, Fractures, Bone physiopathology, Hippocampus pathology, Hippocampus physiopathology, Memory Disorders etiology, Memory Disorders metabolism, Memory Disorders pathology, Memory Disorders physiopathology, Memory, Long-Term, Stroke etiology, Stroke metabolism, Stroke pathology, Stroke physiopathology
- Abstract
Cognitive impairment occurs in stroke and hip fracture patients. In mice, bone fracture (BF) exacerbates stroke-related neuronal damage and sensorimotor dysfunction. We hypothesize that BF exacerbates post-stroke cognitive impairment. Adult mice were randomly assigned into BF, stroke, BF+stroke (BF 6 h before stroke), and control (sham operated) groups. Memory function was evaluated weekly for eight weeks by Y maze test and at eight weeks post-surgeries by novel object recognition (NOR) test. The neuronal damage and inflammation in hippocampus were analyzed three days and eight weeks after the surgeries. In Y maze test, BF+stroke mice started making fewer alternations than controls two weeks after the surgeries. Significant difference between BF+stroke and stroke groups started at five weeks post-injury and continued to the end of the experiment. In NOR test, BF+stroke group spent less time on novel objective than that of other groups. Cx3cr1
+ cells and CD68+ cells accumulated in the stratum lacunosum moleculare (SLM) on the ipsilateral side of stroke injury in stroke and BF+stroke mice. BF+stroke mice had a higher ratio of ipsilateral/contralateral Cx3cr1+ cell-density than that of stroke mice. Therefore, BF shortly before stroke exacerbates hippocampal inflammation and causes long-lasting memory dysfunction.- Published
- 2020
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