Treadmill exercise improves neurological function by inhibiting autophagy and the binding of HMGB1 to Beclin1 in MCAO juvenile rats

Treadmill exercise is a beneficial treatment following childhood stroke. Thus, studies focusing on the neuroprotective mechanism of exercise training during postischemic treatment in children with ischemic stroke are urgently needed. We evaluated the effects of treadmill exercise on autophagy after...

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Veröffentlicht in:Life sciences (1973) 2020-02, Vol.243, p.117279-117279, Article 117279
Hauptverfasser: Pan, Guoyuan, Jin, Lingqin, Shen, Weimin, Zhang, Jieqiong, Pan, Juanjuan, Cheng, Jingyan, Xie, Qingfeng, Hu, Quan, Wu, Shamin, Zhang, Hongmei, Chen, Xiang
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container_title Life sciences (1973)
container_volume 243
creator Pan, Guoyuan
Jin, Lingqin
Shen, Weimin
Zhang, Jieqiong
Pan, Juanjuan
Cheng, Jingyan
Xie, Qingfeng
Hu, Quan
Wu, Shamin
Zhang, Hongmei
Chen, Xiang
description Treadmill exercise is a beneficial treatment following childhood stroke. Thus, studies focusing on the neuroprotective mechanism of exercise training during postischemic treatment in children with ischemic stroke are urgently needed. We evaluated the effects of treadmill exercise on autophagy after cerebral ischemia in young rats. Rats (23–25 days old) underwent cerebral ischemia-reperfusion (CI/R) surgery. The experimental animals were divided into 5 groups, and some groups received either treadmill exercise, a rapamycin (RAPA) injection or combination therapy for 3 or 7 days. We performed a series of experimental tests including neurological scoring, hematoxylin-eosin staining (H&E), Nissl staining, triphenyl tetrazolium chloride (TTC) staining, Western blot analysis (WB), immunofluorescence (IF), enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy (TEM) and Terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) fluorescence. The experimental data indicated that treadmill exercise inhibited autophagy in the ischemic penumbra, inhibited high mobility group box 1 (HMGB1) translocation and binding to Beclin1, reduced apoptosis, reduced infarct volumes, and aided in functional recovery. However, RAPA promoted the opposite effects of treadmill exercise. We found that treadmill exercise improves the neurological deficits induced by CI/R by inhibiting autophagy and HMGB1 binding to Beclin1.
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Thus, studies focusing on the neuroprotective mechanism of exercise training during postischemic treatment in children with ischemic stroke are urgently needed. We evaluated the effects of treadmill exercise on autophagy after cerebral ischemia in young rats. Rats (23–25 days old) underwent cerebral ischemia-reperfusion (CI/R) surgery. The experimental animals were divided into 5 groups, and some groups received either treadmill exercise, a rapamycin (RAPA) injection or combination therapy for 3 or 7 days. We performed a series of experimental tests including neurological scoring, hematoxylin-eosin staining (H&amp;E), Nissl staining, triphenyl tetrazolium chloride (TTC) staining, Western blot analysis (WB), immunofluorescence (IF), enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy (TEM) and Terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) fluorescence. The experimental data indicated that treadmill exercise inhibited autophagy in the ischemic penumbra, inhibited high mobility group box 1 (HMGB1) translocation and binding to Beclin1, reduced apoptosis, reduced infarct volumes, and aided in functional recovery. However, RAPA promoted the opposite effects of treadmill exercise. 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Thus, studies focusing on the neuroprotective mechanism of exercise training during postischemic treatment in children with ischemic stroke are urgently needed. We evaluated the effects of treadmill exercise on autophagy after cerebral ischemia in young rats. Rats (23–25 days old) underwent cerebral ischemia-reperfusion (CI/R) surgery. The experimental animals were divided into 5 groups, and some groups received either treadmill exercise, a rapamycin (RAPA) injection or combination therapy for 3 or 7 days. We performed a series of experimental tests including neurological scoring, hematoxylin-eosin staining (H&amp;E), Nissl staining, triphenyl tetrazolium chloride (TTC) staining, Western blot analysis (WB), immunofluorescence (IF), enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy (TEM) and Terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) fluorescence. The experimental data indicated that treadmill exercise inhibited autophagy in the ischemic penumbra, inhibited high mobility group box 1 (HMGB1) translocation and binding to Beclin1, reduced apoptosis, reduced infarct volumes, and aided in functional recovery. However, RAPA promoted the opposite effects of treadmill exercise. 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Biomedicine</topic><topic>Male</topic><topic>Medicine, Research &amp; Experimental</topic><topic>Neurological diseases</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents</topic><topic>Phagocytosis</topic><topic>Pharmacology &amp; Pharmacy</topic><topic>Physical Conditioning, Animal</topic><topic>Physical training</topic><topic>Protein Binding</topic><topic>Rapamycin</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Recovery of function</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - metabolism</topic><topic>Research &amp; Experimental Medicine</topic><topic>Rodents</topic><topic>Science &amp; Technology</topic><topic>Staining</topic><topic>Stroke</topic><topic>Surgery</topic><topic>Translocation</topic><topic>Transmission electron microscopy</topic><topic>Treadmill exercise</topic><topic>Treadmills</topic><topic>Triphenyltetrazolium chloride</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Pan, Guoyuan</creatorcontrib><creatorcontrib>Jin, Lingqin</creatorcontrib><creatorcontrib>Shen, Weimin</creatorcontrib><creatorcontrib>Zhang, Jieqiong</creatorcontrib><creatorcontrib>Pan, Juanjuan</creatorcontrib><creatorcontrib>Cheng, Jingyan</creatorcontrib><creatorcontrib>Xie, Qingfeng</creatorcontrib><creatorcontrib>Hu, Quan</creatorcontrib><creatorcontrib>Wu, Shamin</creatorcontrib><creatorcontrib>Zhang, Hongmei</creatorcontrib><creatorcontrib>Chen, Xiang</creatorcontrib><collection>Web of Science - Science Citation Index Expanded - 2020</collection><collection>Web of Science Core Collection</collection><collection>Science Citation Index Expanded</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium &amp; 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Thus, studies focusing on the neuroprotective mechanism of exercise training during postischemic treatment in children with ischemic stroke are urgently needed. We evaluated the effects of treadmill exercise on autophagy after cerebral ischemia in young rats. Rats (23–25 days old) underwent cerebral ischemia-reperfusion (CI/R) surgery. The experimental animals were divided into 5 groups, and some groups received either treadmill exercise, a rapamycin (RAPA) injection or combination therapy for 3 or 7 days. We performed a series of experimental tests including neurological scoring, hematoxylin-eosin staining (H&amp;E), Nissl staining, triphenyl tetrazolium chloride (TTC) staining, Western blot analysis (WB), immunofluorescence (IF), enzyme-linked immunosorbent assay (ELISA), transmission electron microscopy (TEM) and Terminal deoxynucleotidyl transferase-mediated dUTP-digoxigenin nick end labeling (TUNEL) fluorescence. The experimental data indicated that treadmill exercise inhibited autophagy in the ischemic penumbra, inhibited high mobility group box 1 (HMGB1) translocation and binding to Beclin1, reduced apoptosis, reduced infarct volumes, and aided in functional recovery. However, RAPA promoted the opposite effects of treadmill exercise. We found that treadmill exercise improves the neurological deficits induced by CI/R by inhibiting autophagy and HMGB1 binding to Beclin1.</abstract><cop>OXFORD</cop><pub>Elsevier Inc</pub><pmid>31926245</pmid><doi>10.1016/j.lfs.2020.117279</doi><tpages>12</tpages></addata></record>
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subjects Animals
Apoptosis
Autophagy
Beclin-1 - metabolism
Binding
Brain - metabolism
Brain - pathology
Brain - physiopathology
Brain Ischemia - metabolism
Childhood stroke
Children
Digoxigenin
DNA nucleotidylexotransferase
Enzyme-linked immunosorbent assay
Fitness equipment
Fluorescence
HMGB1
HMGB1 protein
HMGB1 Protein - metabolism
Immunofluorescence
Ischemia
Life Sciences & Biomedicine
Male
Medicine, Research & Experimental
Neurological diseases
Neuroprotection
Neuroprotective Agents
Phagocytosis
Pharmacology & Pharmacy
Physical Conditioning, Animal
Physical training
Protein Binding
Rapamycin
Rats
Rats, Sprague-Dawley
Recovery of function
Reperfusion
Reperfusion Injury - metabolism
Research & Experimental Medicine
Rodents
Science & Technology
Staining
Stroke
Surgery
Translocation
Transmission electron microscopy
Treadmill exercise
Treadmills
Triphenyltetrazolium chloride
title Treadmill exercise improves neurological function by inhibiting autophagy and the binding of HMGB1 to Beclin1 in MCAO juvenile rats
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