4.2 Article

Physical exercise induces expression of CD31 and facilitates neural function recovery in rats with focal cerebral infarction

Journal

NEUROLOGICAL RESEARCH
Volume 32, Issue 4, Pages 397-402

Publisher

MANEY PUBLISHING
DOI: 10.1179/016164110X12670144526309

Keywords

Cerebral infarction; physical exercise; angiogenesis; neural function; rat

Funding

  1. Foundation of Ministry of Science and Technology of Guangdong Province, China [31751, 8251008901000006]

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Objectives: The present study was aimed at examining the role of physical exercise in the improvement of damaged neural function and the induction of angiogenesis. Methods: An infarction model was induced by ligating the left middle cerebral artery occlusion (MCAO) in a total of 66 adult Sprague-Dawley rats that were further randomly divided into three groups: the physical exercise group (n=30), which was given running wheel exercise every day after MCAO, the control group (n=30) and sham-operated group (n=6), which were fed in standard cages without any special training exercise. The rats were killed on the third, seventh and fourteenth days and the neurological severity scores were examined for evaluating the neural function. And the neogenetic microvessels around the peri-infarction region were checked with the specific marker CD31. Results: Although neogenetic microvessels in the peri-infarction region were observed in both control group and physical exercise group, which showed the highest signal on the seventh day after ischemia, the number of CD31 positive cells significantly increased in physical exercise group in comparison with those in control group on the seventh and fourteenth days after ischemia (p<0.01). Moreover, the neurological severity scores in the physical exercise group showed more quick declination as compared to those in control group from the seventh day after ischemic. Conclusion: Our results suggested that physical exercise plays an important role in the recovery of damaged neural function and induction of angiogenesis after cerebral infarction in rats.

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