Cerebrolysin alleviates cognitive deficits induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins in the rat hippocampus
•Cerebrolysin improved spatial learning and memory impairments in Morris water maze.•Cerebrolysin increases plasticity-related proteins level in the hippocampus of VaD rats.•Cerebrolysin decreases the levels of apoptosis-related proteins in VaD rats. The incidence of vascular dementia (VaD) has rapi...
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| Veröffentlicht in: | Neuroscience letters 2017-06, Vol.651, p.72-78 |
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| creator | Liu, Zhijuan Hu, Ming Lu, Peiyuan Wang, Hebo Qi, Qianqian Xu, Jing Xiao, Yining Fan, Mingyue Jia, Yanqiu Zhang, Dandan |
| description | •Cerebrolysin improved spatial learning and memory impairments in Morris water maze.•Cerebrolysin increases plasticity-related proteins level in the hippocampus of VaD rats.•Cerebrolysin decreases the levels of apoptosis-related proteins in VaD rats.
The incidence of vascular dementia (VaD) has rapidly increased over the past few decades. Although officially approved medications for VaD remain limited, cerebrolysin (CBL) had preventive and treatment effects on VaD in some clinical trials. However, the underlying mechanisms have not been determined. The aim of this study was to determine whether CBL protects against cognitive deficits in a rat model of VaD induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins. In our study, adult male Sprague-Dawley rats were subjected to bilateral common carotid artery occlusion (BCCAO) surgery. The animals were randomly divided into four groups after the operation: Sham, Vehicle, L-CBL (2.5ml/kg), and H-CBL (5ml/kg). CBL was administered after the operation daily for 28 days. The CBL treatment significantly decreased the escape latency and increased the percentage of time the rat spent in the target quadrant of the Morris water maze (MWM) task. Pathological changes in the hippocampus, such as reduced cell count numbers and obvious pyknosis, were observed using haematoxylin–eosin (HE) staining. Furthermore, CBL significantly increased the expression of plasticity-related synaptic proteins, such as postsynaptic density protein 95 (PSD-95), protein kinase C subunit gamma (PKCγ), phosphorylated cAMP response element binding protein (p-CREB), and decreased the expression of apoptosis-related proteins in the hippocampus. In summary, CBL likely protects against cognitive deficits by improving synaptic plasticity and decreasing apoptosis. |
| doi_str_mv | 10.1016/j.neulet.2017.04.022 |
| format | Article |
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The incidence of vascular dementia (VaD) has rapidly increased over the past few decades. Although officially approved medications for VaD remain limited, cerebrolysin (CBL) had preventive and treatment effects on VaD in some clinical trials. However, the underlying mechanisms have not been determined. The aim of this study was to determine whether CBL protects against cognitive deficits in a rat model of VaD induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins. In our study, adult male Sprague-Dawley rats were subjected to bilateral common carotid artery occlusion (BCCAO) surgery. The animals were randomly divided into four groups after the operation: Sham, Vehicle, L-CBL (2.5ml/kg), and H-CBL (5ml/kg). CBL was administered after the operation daily for 28 days. The CBL treatment significantly decreased the escape latency and increased the percentage of time the rat spent in the target quadrant of the Morris water maze (MWM) task. Pathological changes in the hippocampus, such as reduced cell count numbers and obvious pyknosis, were observed using haematoxylin–eosin (HE) staining. Furthermore, CBL significantly increased the expression of plasticity-related synaptic proteins, such as postsynaptic density protein 95 (PSD-95), protein kinase C subunit gamma (PKCγ), phosphorylated cAMP response element binding protein (p-CREB), and decreased the expression of apoptosis-related proteins in the hippocampus. In summary, CBL likely protects against cognitive deficits by improving synaptic plasticity and decreasing apoptosis.</description><identifier>ISSN: 0304-3940</identifier><identifier>EISSN: 1872-7972</identifier><identifier>DOI: 10.1016/j.neulet.2017.04.022</identifier><identifier>PMID: 28458021</identifier><language>eng</language><publisher>Ireland: Elsevier B.V</publisher><subject>Amino Acids - administration & dosage ; Animals ; Apoptosis - drug effects ; Apoptosis-related proteins ; BCCAO ; Cerebrolysin ; Cyclic AMP Response Element-Binding Protein - metabolism ; Dementia, Vascular - drug therapy ; Dementia, Vascular - metabolism ; Dementia, Vascular - pathology ; Dementia, Vascular - psychology ; Disks Large Homolog 4 Protein - metabolism ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; Male ; Neuronal Plasticity - drug effects ; Neuroprotective Agents - administration & dosage ; Plasticity-related proteins ; Rats, Sprague-Dawley ; Spatial Learning - drug effects ; Spatial Memory - drug effects ; Vascular dementia</subject><ispartof>Neuroscience letters, 2017-06, Vol.651, p.72-78</ispartof><rights>2017 Elsevier B.V.</rights><rights>Copyright © 2017 Elsevier B.V. All rights reserved.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c362t-1983c30573d679b3fec822a1b2b42ef4331acf2b8c91ebaad4450a84c5e9ae723</citedby><cites>FETCH-LOGICAL-c362t-1983c30573d679b3fec822a1b2b42ef4331acf2b8c91ebaad4450a84c5e9ae723</cites></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktohtml>$$Uhttps://www.sciencedirect.com/science/article/pii/S0304394017303233$$EHTML$$P50$$Gelsevier$$H</linktohtml><link.rule.ids>314,776,780,3537,27901,27902,65306</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28458021$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Liu, Zhijuan</creatorcontrib><creatorcontrib>Hu, Ming</creatorcontrib><creatorcontrib>Lu, Peiyuan</creatorcontrib><creatorcontrib>Wang, Hebo</creatorcontrib><creatorcontrib>Qi, Qianqian</creatorcontrib><creatorcontrib>Xu, Jing</creatorcontrib><creatorcontrib>Xiao, Yining</creatorcontrib><creatorcontrib>Fan, Mingyue</creatorcontrib><creatorcontrib>Jia, Yanqiu</creatorcontrib><creatorcontrib>Zhang, Dandan</creatorcontrib><title>Cerebrolysin alleviates cognitive deficits induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins in the rat hippocampus</title><title>Neuroscience letters</title><addtitle>Neurosci Lett</addtitle><description>•Cerebrolysin improved spatial learning and memory impairments in Morris water maze.•Cerebrolysin increases plasticity-related proteins level in the hippocampus of VaD rats.•Cerebrolysin decreases the levels of apoptosis-related proteins in VaD rats.
The incidence of vascular dementia (VaD) has rapidly increased over the past few decades. Although officially approved medications for VaD remain limited, cerebrolysin (CBL) had preventive and treatment effects on VaD in some clinical trials. However, the underlying mechanisms have not been determined. The aim of this study was to determine whether CBL protects against cognitive deficits in a rat model of VaD induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins. In our study, adult male Sprague-Dawley rats were subjected to bilateral common carotid artery occlusion (BCCAO) surgery. The animals were randomly divided into four groups after the operation: Sham, Vehicle, L-CBL (2.5ml/kg), and H-CBL (5ml/kg). CBL was administered after the operation daily for 28 days. The CBL treatment significantly decreased the escape latency and increased the percentage of time the rat spent in the target quadrant of the Morris water maze (MWM) task. Pathological changes in the hippocampus, such as reduced cell count numbers and obvious pyknosis, were observed using haematoxylin–eosin (HE) staining. Furthermore, CBL significantly increased the expression of plasticity-related synaptic proteins, such as postsynaptic density protein 95 (PSD-95), protein kinase C subunit gamma (PKCγ), phosphorylated cAMP response element binding protein (p-CREB), and decreased the expression of apoptosis-related proteins in the hippocampus. In summary, CBL likely protects against cognitive deficits by improving synaptic plasticity and decreasing apoptosis.</description><subject>Amino Acids - administration & dosage</subject><subject>Animals</subject><subject>Apoptosis - drug effects</subject><subject>Apoptosis-related proteins</subject><subject>BCCAO</subject><subject>Cerebrolysin</subject><subject>Cyclic AMP Response Element-Binding Protein - metabolism</subject><subject>Dementia, Vascular - drug therapy</subject><subject>Dementia, Vascular - metabolism</subject><subject>Dementia, Vascular - pathology</subject><subject>Dementia, Vascular - psychology</subject><subject>Disks Large Homolog 4 Protein - metabolism</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Male</subject><subject>Neuronal Plasticity - drug effects</subject><subject>Neuroprotective Agents - administration & dosage</subject><subject>Plasticity-related proteins</subject><subject>Rats, Sprague-Dawley</subject><subject>Spatial Learning - drug effects</subject><subject>Spatial Memory - drug effects</subject><subject>Vascular dementia</subject><issn>0304-3940</issn><issn>1872-7972</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><recordid>eNp9kc1u1DAUhS0EotPCGyDkJZsE_2WSbJDQCChSJTawthznpuORxw6-TqU8Ky-DwxQ2CFbefOecK3-EvOKs5ozv357qAIuHXAvG25qpmgnxhOx414qq7VvxlOyYZKqSvWJX5BrxxBhreKOekyvRqaZjgu_IjwMkGFL0K7pAjffw4EwGpDbeB5fdA9ARJmddRurCuFgY6bBSe0wxOEvtr7Tx9LjOcYY0Lehi2AgXbAJTSu9pPgItveCRxonO3mDeCtcqgS9bI51TzOACUhPGMvePoCkLOaLDv3Pl9I1NJtOjm-dozXle8AV5NhmP8PLxvSHfPn74erit7r58-nx4f1dZuRe54n0nrWRNK8d92w9yAtsJYfggBiVgUlJyYycxdLbnMBgzKtUw0ynbQG-gFfKGvLn0lnu-L4BZnx1a8N4EiAtq3vWybzlvuoKqC2pTREww6Tm5s0mr5kxvWvVJX7TqTatmShetJfb6cWEZzjD-Cf32WIB3F6D8VTEISaN1EIotl8BmPUb3_4WfTgS93A</recordid><startdate>20170609</startdate><enddate>20170609</enddate><creator>Liu, Zhijuan</creator><creator>Hu, Ming</creator><creator>Lu, Peiyuan</creator><creator>Wang, Hebo</creator><creator>Qi, Qianqian</creator><creator>Xu, Jing</creator><creator>Xiao, Yining</creator><creator>Fan, Mingyue</creator><creator>Jia, Yanqiu</creator><creator>Zhang, Dandan</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></search><sort><creationdate>20170609</creationdate><title>Cerebrolysin alleviates cognitive deficits induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins in the rat hippocampus</title><author>Liu, Zhijuan ; Hu, Ming ; Lu, Peiyuan ; Wang, Hebo ; Qi, Qianqian ; Xu, Jing ; Xiao, Yining ; Fan, Mingyue ; Jia, Yanqiu ; Zhang, Dandan</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c362t-1983c30573d679b3fec822a1b2b42ef4331acf2b8c91ebaad4450a84c5e9ae723</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Amino Acids - administration & dosage</topic><topic>Animals</topic><topic>Apoptosis - drug effects</topic><topic>Apoptosis-related proteins</topic><topic>BCCAO</topic><topic>Cerebrolysin</topic><topic>Cyclic AMP Response Element-Binding Protein - metabolism</topic><topic>Dementia, Vascular - drug therapy</topic><topic>Dementia, Vascular - metabolism</topic><topic>Dementia, Vascular - pathology</topic><topic>Dementia, Vascular - psychology</topic><topic>Disks Large Homolog 4 Protein - metabolism</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Male</topic><topic>Neuronal Plasticity - drug effects</topic><topic>Neuroprotective Agents - administration & dosage</topic><topic>Plasticity-related proteins</topic><topic>Rats, Sprague-Dawley</topic><topic>Spatial Learning - drug effects</topic><topic>Spatial Memory - drug effects</topic><topic>Vascular dementia</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Liu, Zhijuan</creatorcontrib><creatorcontrib>Hu, Ming</creatorcontrib><creatorcontrib>Lu, Peiyuan</creatorcontrib><creatorcontrib>Wang, Hebo</creatorcontrib><creatorcontrib>Qi, Qianqian</creatorcontrib><creatorcontrib>Xu, Jing</creatorcontrib><creatorcontrib>Xiao, Yining</creatorcontrib><creatorcontrib>Fan, Mingyue</creatorcontrib><creatorcontrib>Jia, Yanqiu</creatorcontrib><creatorcontrib>Zhang, Dandan</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><jtitle>Neuroscience letters</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Liu, Zhijuan</au><au>Hu, Ming</au><au>Lu, Peiyuan</au><au>Wang, Hebo</au><au>Qi, Qianqian</au><au>Xu, Jing</au><au>Xiao, Yining</au><au>Fan, Mingyue</au><au>Jia, Yanqiu</au><au>Zhang, Dandan</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Cerebrolysin alleviates cognitive deficits induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins in the rat hippocampus</atitle><jtitle>Neuroscience letters</jtitle><addtitle>Neurosci Lett</addtitle><date>2017-06-09</date><risdate>2017</risdate><volume>651</volume><spage>72</spage><epage>78</epage><pages>72-78</pages><issn>0304-3940</issn><eissn>1872-7972</eissn><abstract>•Cerebrolysin improved spatial learning and memory impairments in Morris water maze.•Cerebrolysin increases plasticity-related proteins level in the hippocampus of VaD rats.•Cerebrolysin decreases the levels of apoptosis-related proteins in VaD rats.
The incidence of vascular dementia (VaD) has rapidly increased over the past few decades. Although officially approved medications for VaD remain limited, cerebrolysin (CBL) had preventive and treatment effects on VaD in some clinical trials. However, the underlying mechanisms have not been determined. The aim of this study was to determine whether CBL protects against cognitive deficits in a rat model of VaD induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins. In our study, adult male Sprague-Dawley rats were subjected to bilateral common carotid artery occlusion (BCCAO) surgery. The animals were randomly divided into four groups after the operation: Sham, Vehicle, L-CBL (2.5ml/kg), and H-CBL (5ml/kg). CBL was administered after the operation daily for 28 days. The CBL treatment significantly decreased the escape latency and increased the percentage of time the rat spent in the target quadrant of the Morris water maze (MWM) task. Pathological changes in the hippocampus, such as reduced cell count numbers and obvious pyknosis, were observed using haematoxylin–eosin (HE) staining. Furthermore, CBL significantly increased the expression of plasticity-related synaptic proteins, such as postsynaptic density protein 95 (PSD-95), protein kinase C subunit gamma (PKCγ), phosphorylated cAMP response element binding protein (p-CREB), and decreased the expression of apoptosis-related proteins in the hippocampus. In summary, CBL likely protects against cognitive deficits by improving synaptic plasticity and decreasing apoptosis.</abstract><cop>Ireland</cop><pub>Elsevier B.V</pub><pmid>28458021</pmid><doi>10.1016/j.neulet.2017.04.022</doi><tpages>7</tpages></addata></record> |
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| subjects | Amino Acids - administration & dosage Animals Apoptosis - drug effects Apoptosis-related proteins BCCAO Cerebrolysin Cyclic AMP Response Element-Binding Protein - metabolism Dementia, Vascular - drug therapy Dementia, Vascular - metabolism Dementia, Vascular - pathology Dementia, Vascular - psychology Disks Large Homolog 4 Protein - metabolism Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Male Neuronal Plasticity - drug effects Neuroprotective Agents - administration & dosage Plasticity-related proteins Rats, Sprague-Dawley Spatial Learning - drug effects Spatial Memory - drug effects Vascular dementia |
| title | Cerebrolysin alleviates cognitive deficits induced by chronic cerebral hypoperfusion by increasing the levels of plasticity-related proteins and decreasing the levels of apoptosis-related proteins in the rat hippocampus |
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