Pre-existing weakness is critical for the occurrence of postoperative cognitive dysfunction in mice of the same age
Occurrence of postoperative cognitive dysfunction (POCD) is age-dependent and heterogenous. Factors deciding the occurrence of POCD in patients of the same age undergone same surgeries remain unclear. Here we investigated the effects of pre-existing weakness on the occurrence of POCD in mice of the...
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description | Occurrence of postoperative cognitive dysfunction (POCD) is age-dependent and heterogenous. Factors deciding the occurrence of POCD in patients of the same age undergone same surgeries remain unclear. Here we investigated the effects of pre-existing weakness on the occurrence of POCD in mice of the same age. Pre-existing weakness of mice was induced by intraperitoneal injection of lipopolysaccharide (8mg/kg) and was evaluated by physical frailty index (by open field test), neuroinflammation level (by Iba1 immunostaining and inflammatory factors TNF-α and IL-1β), and neuronal activity (by p-CREB immunostaining). POCD was induced by partial hepatolobectomy and was evaluated by puzzle box test and Morris water maze test. The brains were collected to detect the levels of neuroinflammation, synaptophysin and NMDA receptor subunits NR2A, NR2B and NR1 (by western blot), and oxidative stress (by Dihydroethidium). Compared to the normal adult mice of the same age, LPS pretreated mice had increased physical frailty index, higher levels of neuroinflammation, and lower neuronal activity. Partial hepatolobectomy induced obvious impairments in executive function, learning and memory in LPS pretreated mice after surgery, but not in normal mice of the same age. Partial hepatolobectomy also induced heightened neuroinflammation, obvious loss of NMDA receptor subunits, strong oxidative stress in LPS pretreated mice on the 1st and 3rd postoperative day. However, the POCD-associated pathological changes didn't occur in normal mice of the same age after surgery. These results suggest that pre-existing weakness is critical for the occurrence of POCD in mice of the same age. |
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Factors deciding the occurrence of POCD in patients of the same age undergone same surgeries remain unclear. Here we investigated the effects of pre-existing weakness on the occurrence of POCD in mice of the same age. Pre-existing weakness of mice was induced by intraperitoneal injection of lipopolysaccharide (8mg/kg) and was evaluated by physical frailty index (by open field test), neuroinflammation level (by Iba1 immunostaining and inflammatory factors TNF-α and IL-1β), and neuronal activity (by p-CREB immunostaining). POCD was induced by partial hepatolobectomy and was evaluated by puzzle box test and Morris water maze test. The brains were collected to detect the levels of neuroinflammation, synaptophysin and NMDA receptor subunits NR2A, NR2B and NR1 (by western blot), and oxidative stress (by Dihydroethidium). Compared to the normal adult mice of the same age, LPS pretreated mice had increased physical frailty index, higher levels of neuroinflammation, and lower neuronal activity. Partial hepatolobectomy induced obvious impairments in executive function, learning and memory in LPS pretreated mice after surgery, but not in normal mice of the same age. Partial hepatolobectomy also induced heightened neuroinflammation, obvious loss of NMDA receptor subunits, strong oxidative stress in LPS pretreated mice on the 1st and 3rd postoperative day. However, the POCD-associated pathological changes didn't occur in normal mice of the same age after surgery. These results suggest that pre-existing weakness is critical for the occurrence of POCD in mice of the same age.</description><identifier>ISSN: 1932-6203</identifier><identifier>EISSN: 1932-6203</identifier><identifier>DOI: 10.1371/journal.pone.0182471</identifier><identifier>PMID: 28787017</identifier><language>eng</language><publisher>United States: Public Library of Science</publisher><subject>Age ; Anesthesiology ; Animal cognition ; Animals ; Biology and Life Sciences ; Brain research ; Cognitive ability ; Cognitive disorders ; Cognitive Dysfunction - metabolism ; Cognitive Dysfunction - physiopathology ; Cyclic AMP response element-binding protein ; Disease Susceptibility ; Executive function ; Experiments ; Gene expression ; Glutamic acid receptors (ionotropic) ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - physiopathology ; House mouse ; Inflammation ; Injection ; Interleukin 1 ; Learning ; Lipopolysaccharides ; Lipopolysaccharides - pharmacology ; Male ; Medicine and Health Sciences ; Memory ; Mice ; Mice, Inbred C57BL ; Mortality ; N-Methyl-D-aspartic acid receptors ; Open-field behavior ; Oxidative stress ; Patients ; Postoperative complications ; Postoperative Complications - metabolism ; Postoperative Complications - physiopathology ; Reactive Oxygen Species - metabolism ; Receptors, N-Methyl-D-Aspartate - metabolism ; Research and Analysis Methods ; Risk factors ; Rodents ; Studies ; Surgery ; Synaptophysin ; Tumor necrosis factor</subject><ispartof>PloS one, 2017-08, Vol.12 (8), p.e0182471-e0182471</ispartof><rights>COPYRIGHT 2017 Public Library of Science</rights><rights>2017 Tang et al. This is an open access article distributed under the terms of the Creative Commons Attribution License: http://creativecommons.org/licenses/by/4.0/ (the “License”), which permits unrestricted use, distribution, and reproduction in any medium, provided the original author and source are credited. Notwithstanding the ProQuest Terms and Conditions, you may use this content in accordance with the terms of the License.</rights><rights>2017 Tang et al 2017 Tang et al</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c758t-7220b674822249abbbe0b6c4e477c51b254c8b199d3fcdac5b0c89c222089b6f3</citedby><cites>FETCH-LOGICAL-c758t-7220b674822249abbbe0b6c4e477c51b254c8b199d3fcdac5b0c89c222089b6f3</cites><orcidid>0000-0002-0062-3318</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5546624/pdf/$$EPDF$$P50$$Gpubmedcentral$$Hfree_for_read</linktopdf><linktohtml>$$Uhttps://www.ncbi.nlm.nih.gov/pmc/articles/PMC5546624/$$EHTML$$P50$$Gpubmedcentral$$Hfree_for_read</linktohtml><link.rule.ids>230,314,724,777,781,861,882,2096,2915,23847,27905,27906,53772,53774,79349,79350</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/28787017$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><contributor>Zuo, Zhiyi</contributor><creatorcontrib>Tang, Yujie</creatorcontrib><creatorcontrib>Wang, Xueqin</creatorcontrib><creatorcontrib>Zhang, Shuibing</creatorcontrib><creatorcontrib>Duan, Shangchun</creatorcontrib><creatorcontrib>Qing, Wenxiang</creatorcontrib><creatorcontrib>Chen, Gong</creatorcontrib><creatorcontrib>Ye, Feng</creatorcontrib><creatorcontrib>Le, Yuan</creatorcontrib><creatorcontrib>Ouyang, Wen</creatorcontrib><title>Pre-existing weakness is critical for the occurrence of postoperative cognitive dysfunction in mice of the same age</title><title>PloS one</title><addtitle>PLoS One</addtitle><description>Occurrence of postoperative cognitive dysfunction (POCD) is age-dependent and heterogenous. Factors deciding the occurrence of POCD in patients of the same age undergone same surgeries remain unclear. Here we investigated the effects of pre-existing weakness on the occurrence of POCD in mice of the same age. Pre-existing weakness of mice was induced by intraperitoneal injection of lipopolysaccharide (8mg/kg) and was evaluated by physical frailty index (by open field test), neuroinflammation level (by Iba1 immunostaining and inflammatory factors TNF-α and IL-1β), and neuronal activity (by p-CREB immunostaining). POCD was induced by partial hepatolobectomy and was evaluated by puzzle box test and Morris water maze test. The brains were collected to detect the levels of neuroinflammation, synaptophysin and NMDA receptor subunits NR2A, NR2B and NR1 (by western blot), and oxidative stress (by Dihydroethidium). Compared to the normal adult mice of the same age, LPS pretreated mice had increased physical frailty index, higher levels of neuroinflammation, and lower neuronal activity. Partial hepatolobectomy induced obvious impairments in executive function, learning and memory in LPS pretreated mice after surgery, but not in normal mice of the same age. Partial hepatolobectomy also induced heightened neuroinflammation, obvious loss of NMDA receptor subunits, strong oxidative stress in LPS pretreated mice on the 1st and 3rd postoperative day. However, the POCD-associated pathological changes didn't occur in normal mice of the same age after surgery. These results suggest that pre-existing weakness is critical for the occurrence of POCD in mice of the same age.</description><subject>Age</subject><subject>Anesthesiology</subject><subject>Animal cognition</subject><subject>Animals</subject><subject>Biology and Life Sciences</subject><subject>Brain research</subject><subject>Cognitive ability</subject><subject>Cognitive disorders</subject><subject>Cognitive Dysfunction - metabolism</subject><subject>Cognitive Dysfunction - physiopathology</subject><subject>Cyclic AMP response element-binding protein</subject><subject>Disease Susceptibility</subject><subject>Executive function</subject><subject>Experiments</subject><subject>Gene expression</subject><subject>Glutamic acid receptors (ionotropic)</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - physiopathology</subject><subject>House mouse</subject><subject>Inflammation</subject><subject>Injection</subject><subject>Interleukin 1</subject><subject>Learning</subject><subject>Lipopolysaccharides</subject><subject>Lipopolysaccharides - pharmacology</subject><subject>Male</subject><subject>Medicine and Health Sciences</subject><subject>Memory</subject><subject>Mice</subject><subject>Mice, Inbred C57BL</subject><subject>Mortality</subject><subject>N-Methyl-D-aspartic acid receptors</subject><subject>Open-field behavior</subject><subject>Oxidative stress</subject><subject>Patients</subject><subject>Postoperative complications</subject><subject>Postoperative Complications - metabolism</subject><subject>Postoperative Complications - physiopathology</subject><subject>Reactive Oxygen Species - metabolism</subject><subject>Receptors, N-Methyl-D-Aspartate - metabolism</subject><subject>Research and Analysis Methods</subject><subject>Risk factors</subject><subject>Rodents</subject><subject>Studies</subject><subject>Surgery</subject><subject>Synaptophysin</subject><subject>Tumor necrosis factor</subject><issn>1932-6203</issn><issn>1932-6203</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2017</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>AZQEC</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><sourceid>DWQXO</sourceid><sourceid>GNUQQ</sourceid><sourceid>DOA</sourceid><recordid>eNqNk0tv1DAQxyMEoqXwDRBEQkJw2MWv2MkFqap4rFSpiNfVcpxJ1iVrL7ZT2m-Ps5tWG9QD8sFj-zf_scczWfYcoyWmAr-7dIO3ql9unYUlwiVhAj_IjnFFyYITRB8e2EfZkxAuESpoyfnj7IiUohQIi-MsfPGwgGsTorFd_gfULwsh5Cbk2ptotOrz1vk8riF3Wg_eg9XJbPOtC9FtwatoriDXrrNmZzU3oR2sjsbZ3Nh8Y_b4KBDUBnLVwdPsUav6AM-m-ST78fHD97PPi_OLT6uz0_OFFkUZF4IQVHPBSkIIq1Rd15DWmgETQhe4JgXTZY2rqqGtbpQuaqTLSicalVXNW3qSvdzrbnsX5JSvIHFFeFkJLIpErPZE49Sl3HqzUf5GOmXkbsP5TiqfstCDpKVGRFdas6pkBLU1o5TzplAYi4YKkrTeT9GGegONBhu96mei8xNr1rJzV7IoGOeEJYE3k4B3vwcIUW5M0ND3yoIbdvcWFPGC8IS--ge9_3UT1an0AGNbl-LqUVSeFihVAyJoDLu8h0qjgfR5qbhak_ZnDm9nDomJcB07NYQgV9--_j978XPOvj5g16D6uA6uH8ZSCnOQ7UHtXQge2rskYyTH3rjNhhx7Q069kdxeHH7QndNtM9C_W-YJdg</recordid><startdate>20170807</startdate><enddate>20170807</enddate><creator>Tang, Yujie</creator><creator>Wang, Xueqin</creator><creator>Zhang, Shuibing</creator><creator>Duan, Shangchun</creator><creator>Qing, Wenxiang</creator><creator>Chen, Gong</creator><creator>Ye, Feng</creator><creator>Le, Yuan</creator><creator>Ouyang, Wen</creator><general>Public Library of Science</general><general>Public Library of Science (PLoS)</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>IOV</scope><scope>ISR</scope><scope>3V.</scope><scope>7QG</scope><scope>7QL</scope><scope>7QO</scope><scope>7RV</scope><scope>7SN</scope><scope>7SS</scope><scope>7T5</scope><scope>7TG</scope><scope>7TM</scope><scope>7U9</scope><scope>7X2</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8C1</scope><scope>8FD</scope><scope>8FE</scope><scope>8FG</scope><scope>8FH</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABJCF</scope><scope>ABUWG</scope><scope>AEUYN</scope><scope>AFKRA</scope><scope>ARAPS</scope><scope>ATCPS</scope><scope>AZQEC</scope><scope>BBNVY</scope><scope>BENPR</scope><scope>BGLVJ</scope><scope>BHPHI</scope><scope>C1K</scope><scope>CCPQU</scope><scope>D1I</scope><scope>DWQXO</scope><scope>FR3</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>GNUQQ</scope><scope>H94</scope><scope>HCIFZ</scope><scope>K9.</scope><scope>KB.</scope><scope>KB0</scope><scope>KL.</scope><scope>L6V</scope><scope>LK8</scope><scope>M0K</scope><scope>M0S</scope><scope>M1P</scope><scope>M7N</scope><scope>M7P</scope><scope>M7S</scope><scope>NAPCQ</scope><scope>P5Z</scope><scope>P62</scope><scope>P64</scope><scope>PATMY</scope><scope>PDBOC</scope><scope>PIMPY</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PTHSS</scope><scope>PYCSY</scope><scope>RC3</scope><scope>7X8</scope><scope>5PM</scope><scope>DOA</scope><orcidid>https://orcid.org/0000-0002-0062-3318</orcidid></search><sort><creationdate>20170807</creationdate><title>Pre-existing weakness is critical for the occurrence of postoperative cognitive dysfunction in mice of the same age</title><author>Tang, Yujie ; Wang, Xueqin ; Zhang, Shuibing ; Duan, Shangchun ; Qing, Wenxiang ; Chen, Gong ; Ye, Feng ; Le, Yuan ; Ouyang, Wen</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c758t-7220b674822249abbbe0b6c4e477c51b254c8b199d3fcdac5b0c89c222089b6f3</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2017</creationdate><topic>Age</topic><topic>Anesthesiology</topic><topic>Animal cognition</topic><topic>Animals</topic><topic>Biology and Life Sciences</topic><topic>Brain research</topic><topic>Cognitive ability</topic><topic>Cognitive disorders</topic><topic>Cognitive Dysfunction - 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Factors deciding the occurrence of POCD in patients of the same age undergone same surgeries remain unclear. Here we investigated the effects of pre-existing weakness on the occurrence of POCD in mice of the same age. Pre-existing weakness of mice was induced by intraperitoneal injection of lipopolysaccharide (8mg/kg) and was evaluated by physical frailty index (by open field test), neuroinflammation level (by Iba1 immunostaining and inflammatory factors TNF-α and IL-1β), and neuronal activity (by p-CREB immunostaining). POCD was induced by partial hepatolobectomy and was evaluated by puzzle box test and Morris water maze test. The brains were collected to detect the levels of neuroinflammation, synaptophysin and NMDA receptor subunits NR2A, NR2B and NR1 (by western blot), and oxidative stress (by Dihydroethidium). Compared to the normal adult mice of the same age, LPS pretreated mice had increased physical frailty index, higher levels of neuroinflammation, and lower neuronal activity. Partial hepatolobectomy induced obvious impairments in executive function, learning and memory in LPS pretreated mice after surgery, but not in normal mice of the same age. Partial hepatolobectomy also induced heightened neuroinflammation, obvious loss of NMDA receptor subunits, strong oxidative stress in LPS pretreated mice on the 1st and 3rd postoperative day. However, the POCD-associated pathological changes didn't occur in normal mice of the same age after surgery. These results suggest that pre-existing weakness is critical for the occurrence of POCD in mice of the same age.</abstract><cop>United States</cop><pub>Public Library of Science</pub><pmid>28787017</pmid><doi>10.1371/journal.pone.0182471</doi><tpages>e0182471</tpages><orcidid>https://orcid.org/0000-0002-0062-3318</orcidid><oa>free_for_read</oa></addata></record> |
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source | MEDLINE; DOAJ Directory of Open Access Journals; Public Library of Science (PLoS); EZB-FREE-00999 freely available EZB journals; PubMed Central; Free Full-Text Journals in Chemistry |
subjects | Age Anesthesiology Animal cognition Animals Biology and Life Sciences Brain research Cognitive ability Cognitive disorders Cognitive Dysfunction - metabolism Cognitive Dysfunction - physiopathology Cyclic AMP response element-binding protein Disease Susceptibility Executive function Experiments Gene expression Glutamic acid receptors (ionotropic) Hippocampus - drug effects Hippocampus - metabolism Hippocampus - physiopathology House mouse Inflammation Injection Interleukin 1 Learning Lipopolysaccharides Lipopolysaccharides - pharmacology Male Medicine and Health Sciences Memory Mice Mice, Inbred C57BL Mortality N-Methyl-D-aspartic acid receptors Open-field behavior Oxidative stress Patients Postoperative complications Postoperative Complications - metabolism Postoperative Complications - physiopathology Reactive Oxygen Species - metabolism Receptors, N-Methyl-D-Aspartate - metabolism Research and Analysis Methods Risk factors Rodents Studies Surgery Synaptophysin Tumor necrosis factor |
title | Pre-existing weakness is critical for the occurrence of postoperative cognitive dysfunction in mice of the same age |
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