The neuroprotective effects of preconditioning exercise on brain damage and neurotrophic factors after focal brain ischemia in rats
•Preconditioning exercise prior to ischemia reduced infract volume and sensorimotor deficits.•MK and BDNF expression levels were upregulated by preconditioning exercise after stroke.•Preconditioning exercise activated astrocytes and promoted angiogenesis after stroke.•Preconditioning exercise reduce...
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| Veröffentlicht in: | Behavioural brain research 2016-04, Vol.303, p.9-18 |
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| creator | Otsuka, Shotaro Sakakima, Harutoshi Sumizono, Megumi Takada, Seiya Terashi, Takuto Yoshida, Yoshihiro |
| description | •Preconditioning exercise prior to ischemia reduced infract volume and sensorimotor deficits.•MK and BDNF expression levels were upregulated by preconditioning exercise after stroke.•Preconditioning exercise activated astrocytes and promoted angiogenesis after stroke.•Preconditioning exercise reduced apoptotic activity and oxidative damage in neuronal cells.
Preconditioning exercise can exert neuroprotective effects after stroke. However, the mechanism underlying these neuroprotective effects by preconditioning exercise remains unclear. We investigated the neuroprotective effects of preconditioning exercise on brain damage and the expression levels of the midkine (MK) and brain-derived neurotrophic factor (BDNF) after brain ischemia. Animals were assigned to one of 4 groups: exercise and ischemia (Ex), no exercise and ischemia (No-Ex), exercise and no ischemia (Ex-only), and no exercise and intact (Control). Rats ran on a treadmill for 30min once a day at a speed of 25m/min for 5days a week for 3 weeks. After the exercise program, stroke was induced by a 60min left middle cerebral artery occlusion using an intraluminal filament. The infarct volume, motor function, neurological deficits, and the cellular expressions levels of MK, BDNF, GFAP, PECAM-1, caspase 3, and nitrotyrosine (NT) were evaluated 48h after the induction of ischemia. The infarct volume, neurological deficits and motor function in the Ex group were significantly improved compared to that of the No-Ex group. The expression levels of MK, BDNF, GFAP, and PECAM-1 were enhanced in the Ex group compared to the expression levels in the No-Ex group after brain ischemia, while the expression levels of activated caspase 3 and NT were reduced in the area surrounding the necrotic lesion. Our findings suggest that preconditioning exercise reduced the infract volume and ameliorated motor function, enhanced expression levels of MK and BDNF, increased astrocyte proliferation, increased angiogenesis, and reduced neuronal apoptosis and oxidative stress. |
| doi_str_mv | 10.1016/j.bbr.2016.01.049 |
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Preconditioning exercise can exert neuroprotective effects after stroke. However, the mechanism underlying these neuroprotective effects by preconditioning exercise remains unclear. We investigated the neuroprotective effects of preconditioning exercise on brain damage and the expression levels of the midkine (MK) and brain-derived neurotrophic factor (BDNF) after brain ischemia. Animals were assigned to one of 4 groups: exercise and ischemia (Ex), no exercise and ischemia (No-Ex), exercise and no ischemia (Ex-only), and no exercise and intact (Control). Rats ran on a treadmill for 30min once a day at a speed of 25m/min for 5days a week for 3 weeks. After the exercise program, stroke was induced by a 60min left middle cerebral artery occlusion using an intraluminal filament. The infarct volume, motor function, neurological deficits, and the cellular expressions levels of MK, BDNF, GFAP, PECAM-1, caspase 3, and nitrotyrosine (NT) were evaluated 48h after the induction of ischemia. The infarct volume, neurological deficits and motor function in the Ex group were significantly improved compared to that of the No-Ex group. The expression levels of MK, BDNF, GFAP, and PECAM-1 were enhanced in the Ex group compared to the expression levels in the No-Ex group after brain ischemia, while the expression levels of activated caspase 3 and NT were reduced in the area surrounding the necrotic lesion. Our findings suggest that preconditioning exercise reduced the infract volume and ameliorated motor function, enhanced expression levels of MK and BDNF, increased astrocyte proliferation, increased angiogenesis, and reduced neuronal apoptosis and oxidative stress.</description><identifier>ISSN: 0166-4328</identifier><identifier>EISSN: 1872-7549</identifier><identifier>DOI: 10.1016/j.bbr.2016.01.049</identifier><identifier>PMID: 26808606</identifier><language>eng</language><publisher>Netherlands: Elsevier B.V</publisher><subject>Animals ; BDNF ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain-Derived Neurotrophic Factor - metabolism ; Caspase 3 - metabolism ; Cytokines - metabolism ; Glial Fibrillary Acidic Protein - metabolism ; Infarction, Middle Cerebral Artery - metabolism ; Male ; Midkine ; Nerve Growth Factors - metabolism ; Neuroprotection ; Oxidative stress ; Physical Conditioning, Animal ; Platelet Endothelial Cell Adhesion Molecule-1 - metabolism ; Preconditioning exercise ; Rats ; Rats, Sprague-Dawley ; Stroke ; Tyrosine - analogs & derivatives ; Tyrosine - metabolism</subject><ispartof>Behavioural brain research, 2016-04, Vol.303, p.9-18</ispartof><rights>2016 Elsevier B.V.</rights><rights>Copyright © 2016 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c452t-88003c7bffae63330214407748ec2e3bd459d9203a96fbd0c00e75bcdf243be23</citedby><cites>FETCH-LOGICAL-c452t-88003c7bffae63330214407748ec2e3bd459d9203a96fbd0c00e75bcdf243be23</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://dx.doi.org/10.1016/j.bbr.2016.01.049$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,780,784,3550,27924,27925,45995</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/26808606$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Otsuka, Shotaro</creatorcontrib><creatorcontrib>Sakakima, Harutoshi</creatorcontrib><creatorcontrib>Sumizono, Megumi</creatorcontrib><creatorcontrib>Takada, Seiya</creatorcontrib><creatorcontrib>Terashi, Takuto</creatorcontrib><creatorcontrib>Yoshida, Yoshihiro</creatorcontrib><title>The neuroprotective effects of preconditioning exercise on brain damage and neurotrophic factors after focal brain ischemia in rats</title><title>Behavioural brain research</title><addtitle>Behav Brain Res</addtitle><description>•Preconditioning exercise prior to ischemia reduced infract volume and sensorimotor deficits.•MK and BDNF expression levels were upregulated by preconditioning exercise after stroke.•Preconditioning exercise activated astrocytes and promoted angiogenesis after stroke.•Preconditioning exercise reduced apoptotic activity and oxidative damage in neuronal cells.
Preconditioning exercise can exert neuroprotective effects after stroke. However, the mechanism underlying these neuroprotective effects by preconditioning exercise remains unclear. We investigated the neuroprotective effects of preconditioning exercise on brain damage and the expression levels of the midkine (MK) and brain-derived neurotrophic factor (BDNF) after brain ischemia. Animals were assigned to one of 4 groups: exercise and ischemia (Ex), no exercise and ischemia (No-Ex), exercise and no ischemia (Ex-only), and no exercise and intact (Control). Rats ran on a treadmill for 30min once a day at a speed of 25m/min for 5days a week for 3 weeks. After the exercise program, stroke was induced by a 60min left middle cerebral artery occlusion using an intraluminal filament. The infarct volume, motor function, neurological deficits, and the cellular expressions levels of MK, BDNF, GFAP, PECAM-1, caspase 3, and nitrotyrosine (NT) were evaluated 48h after the induction of ischemia. The infarct volume, neurological deficits and motor function in the Ex group were significantly improved compared to that of the No-Ex group. The expression levels of MK, BDNF, GFAP, and PECAM-1 were enhanced in the Ex group compared to the expression levels in the No-Ex group after brain ischemia, while the expression levels of activated caspase 3 and NT were reduced in the area surrounding the necrotic lesion. Our findings suggest that preconditioning exercise reduced the infract volume and ameliorated motor function, enhanced expression levels of MK and BDNF, increased astrocyte proliferation, increased angiogenesis, and reduced neuronal apoptosis and oxidative stress.</description><subject>Animals</subject><subject>BDNF</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain-Derived Neurotrophic Factor - metabolism</subject><subject>Caspase 3 - metabolism</subject><subject>Cytokines - metabolism</subject><subject>Glial Fibrillary Acidic Protein - metabolism</subject><subject>Infarction, Middle Cerebral Artery - metabolism</subject><subject>Male</subject><subject>Midkine</subject><subject>Nerve Growth Factors - metabolism</subject><subject>Neuroprotection</subject><subject>Oxidative stress</subject><subject>Physical Conditioning, Animal</subject><subject>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</subject><subject>Preconditioning exercise</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Stroke</subject><subject>Tyrosine - analogs & derivatives</subject><subject>Tyrosine - metabolism</subject><issn>0166-4328</issn><issn>1872-7549</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2016</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNqNkT9vFDEQxS0EIpfAB6BBLml2Gf_Z9a6oUBQIUiSaUFtee5zz6dY-bF8ENV8cR3dQIio_ye89zcyPkDcMegZsfL_rlyX3vMkeWA9yfkY2bFK8U4Ocn5NN-xg7Kfh0QS5L2QGAhIG9JBd8nGAaYdyQX_dbpBGPOR1yqmhreESK3jdVaPL0kNGm6EINKYb4QPEHZhsK0hTpkk2I1JnVPCA10Z16aqvaBku9sTXlQo2vmKlP1uzPiVDsFtdgaNPZ1PKKvPBmX_D1-b0i3z7d3F_fdndfP3-5_njXWTnw2k0TgLBq8d7gKIQAzqQEpeSElqNYnBxmN3MQZh794sACoBoW6zyXYkEursi7U29b9fsRS9VrGwX3exMxHYtmSomJK8H_ywqTmsdZNCs7WW1OpWT0-pDDavJPzUA_YdI73TDpJ0wamG6YWubtuf64rOj-Jv5waYYPJwO2ezwGzLrYgNGiCw1I1S6Ff9T_Bi9KpNw</recordid><startdate>20160415</startdate><enddate>20160415</enddate><creator>Otsuka, Shotaro</creator><creator>Sakakima, Harutoshi</creator><creator>Sumizono, Megumi</creator><creator>Takada, Seiya</creator><creator>Terashi, Takuto</creator><creator>Yoshida, Yoshihiro</creator><general>Elsevier B.V</general><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7X8</scope><scope>7QG</scope><scope>7TK</scope></search><sort><creationdate>20160415</creationdate><title>The neuroprotective effects of preconditioning exercise on brain damage and neurotrophic factors after focal brain ischemia in rats</title><author>Otsuka, Shotaro ; Sakakima, Harutoshi ; Sumizono, Megumi ; Takada, Seiya ; Terashi, Takuto ; Yoshida, Yoshihiro</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c452t-88003c7bffae63330214407748ec2e3bd459d9203a96fbd0c00e75bcdf243be23</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2016</creationdate><topic>Animals</topic><topic>BDNF</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Brain-Derived Neurotrophic Factor - metabolism</topic><topic>Caspase 3 - metabolism</topic><topic>Cytokines - metabolism</topic><topic>Glial Fibrillary Acidic Protein - metabolism</topic><topic>Infarction, Middle Cerebral Artery - metabolism</topic><topic>Male</topic><topic>Midkine</topic><topic>Nerve Growth Factors - metabolism</topic><topic>Neuroprotection</topic><topic>Oxidative stress</topic><topic>Physical Conditioning, Animal</topic><topic>Platelet Endothelial Cell Adhesion Molecule-1 - metabolism</topic><topic>Preconditioning exercise</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Stroke</topic><topic>Tyrosine - analogs & derivatives</topic><topic>Tyrosine - metabolism</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Otsuka, Shotaro</creatorcontrib><creatorcontrib>Sakakima, Harutoshi</creatorcontrib><creatorcontrib>Sumizono, Megumi</creatorcontrib><creatorcontrib>Takada, Seiya</creatorcontrib><creatorcontrib>Terashi, Takuto</creatorcontrib><creatorcontrib>Yoshida, Yoshihiro</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>MEDLINE - Academic</collection><collection>Animal Behavior Abstracts</collection><collection>Neurosciences Abstracts</collection><jtitle>Behavioural brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Otsuka, Shotaro</au><au>Sakakima, Harutoshi</au><au>Sumizono, Megumi</au><au>Takada, Seiya</au><au>Terashi, Takuto</au><au>Yoshida, Yoshihiro</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>The neuroprotective effects of preconditioning exercise on brain damage and neurotrophic factors after focal brain ischemia in rats</atitle><jtitle>Behavioural brain research</jtitle><addtitle>Behav Brain Res</addtitle><date>2016-04-15</date><risdate>2016</risdate><volume>303</volume><spage>9</spage><epage>18</epage><pages>9-18</pages><issn>0166-4328</issn><eissn>1872-7549</eissn><abstract>•Preconditioning exercise prior to ischemia reduced infract volume and sensorimotor deficits.•MK and BDNF expression levels were upregulated by preconditioning exercise after stroke.•Preconditioning exercise activated astrocytes and promoted angiogenesis after stroke.•Preconditioning exercise reduced apoptotic activity and oxidative damage in neuronal cells.
Preconditioning exercise can exert neuroprotective effects after stroke. However, the mechanism underlying these neuroprotective effects by preconditioning exercise remains unclear. We investigated the neuroprotective effects of preconditioning exercise on brain damage and the expression levels of the midkine (MK) and brain-derived neurotrophic factor (BDNF) after brain ischemia. Animals were assigned to one of 4 groups: exercise and ischemia (Ex), no exercise and ischemia (No-Ex), exercise and no ischemia (Ex-only), and no exercise and intact (Control). Rats ran on a treadmill for 30min once a day at a speed of 25m/min for 5days a week for 3 weeks. After the exercise program, stroke was induced by a 60min left middle cerebral artery occlusion using an intraluminal filament. The infarct volume, motor function, neurological deficits, and the cellular expressions levels of MK, BDNF, GFAP, PECAM-1, caspase 3, and nitrotyrosine (NT) were evaluated 48h after the induction of ischemia. The infarct volume, neurological deficits and motor function in the Ex group were significantly improved compared to that of the No-Ex group. The expression levels of MK, BDNF, GFAP, and PECAM-1 were enhanced in the Ex group compared to the expression levels in the No-Ex group after brain ischemia, while the expression levels of activated caspase 3 and NT were reduced in the area surrounding the necrotic lesion. Our findings suggest that preconditioning exercise reduced the infract volume and ameliorated motor function, enhanced expression levels of MK and BDNF, increased astrocyte proliferation, increased angiogenesis, and reduced neuronal apoptosis and oxidative stress.</abstract><cop>Netherlands</cop><pub>Elsevier B.V</pub><pmid>26808606</pmid><doi>10.1016/j.bbr.2016.01.049</doi><tpages>10</tpages></addata></record> |
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| subjects | Animals BDNF Brain Ischemia - metabolism Brain Ischemia - pathology Brain-Derived Neurotrophic Factor - metabolism Caspase 3 - metabolism Cytokines - metabolism Glial Fibrillary Acidic Protein - metabolism Infarction, Middle Cerebral Artery - metabolism Male Midkine Nerve Growth Factors - metabolism Neuroprotection Oxidative stress Physical Conditioning, Animal Platelet Endothelial Cell Adhesion Molecule-1 - metabolism Preconditioning exercise Rats Rats, Sprague-Dawley Stroke Tyrosine - analogs & derivatives Tyrosine - metabolism |
| title | The neuroprotective effects of preconditioning exercise on brain damage and neurotrophic factors after focal brain ischemia in rats |
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