title: Physical exercise promotes recovery of neurological function after ischemic stroke in rats.
abstract: Although physical exercise is an effective strategy for treatment of ischemic stroke, the underlying protective mechanisms are still not well understood. It has been recently demonstrated that neural progenitor cells play a vital role in the recovery of neurological function (NF) through differentiation into mature neurons. In the current study, we observed that physical exercise significantly reduced the infarct size and improved damaged neural functional recovery after an ischemic stroke. Furthermore, we found that the treatment not only exhibited a significant increase in the number of neural progenitor cells and neurons but also decreased the apoptotic cells in the peri-infarct region, compared to a control in the absence of exercise. Importantly, the insulin-like growth factor-1 (IGF-1)/Akt signaling pathway was dramatically activated in the peri-infarct region of rats after physical exercise training. Therefore, our findings suggest that physical exercise directly influences the NF recovery process by increasing neural progenitor cell count via activation of the IGF-1/Akt signaling pathway.
authors.affiliation: Department of Rehabilitation Medicine Science, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. zhenghq9@gmail.com.
authors.forename: Hai-Qing
authors.initials: HQ
authors.lastname: Zheng
authors.affiliation: Department of Rehabilitation Medicine Science, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. zhangliying_good@126.com.
authors.forename: Li-Ying
authors.initials: LY
authors.lastname: Zhang
authors.affiliation: Department of Rehabilitation Medicine Science, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. jill_272@foxmail.com.
authors.forename: Jing
authors.initials: J
authors.lastname: Luo
authors.affiliation: Department of Rehabilitation Medicine Science, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. ovelyxt2008@163.com.
authors.forename: Li-Li
authors.initials: LL
authors.lastname: Li
authors.affiliation: Department of Rehabilitation Medicine Science, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. serlin313@hotmail.com.
authors.forename: Menglin
authors.initials: M
authors.lastname: Li
authors.affiliation: Department of Rehabilitation Medicine Science, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. zhangqingjie3415@163.com.
authors.forename: Qingjie
authors.initials: Q
authors.lastname: Zhang
authors.affiliation: Department of Rehabilitation Medicine Science, the Third Affiliated Hospital of Sun Yat-sen University, Guangzhou 510630, China. xiquhu@hotmail.com.
authors.forename: Xi-Quan
authors.initials: XQ
authors.lastname: Hu
mesh_terms: D000818:Animals; D017209:Apoptosis; D004195:Disease Models, Animal; D007334:Insulin-Like Growth Factor I / Q000378:metabolism; D008297:Male; D058953:Neural Stem Cells / Q000166:cytology / Q000378:metabolism; D009474:Neurons / Q000378:metabolism*; D010805:Physical Conditioning, Animal; D051057:Proto-Oncogene Proteins c-akt / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D020127:Recovery of Function; D015398:Signal Transduction; D020521:Stroke / Q000378:metabolism / Q000503:physiopathology*
chemical_list: D007334:Insulin-Like Growth Factor I; D051057:Proto-Oncogene Proteins c-akt