Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K–AKT pathway by bioinformatic analysis
Ischemic stroke is one of the most vital causes of high neurological morbidity and mortality in the world. Preconditioning exercise is considered as the primary prevention of stroke to resistance to subsequent injury. We tried to research the underlying biological mechanisms of this exercise. Forty-...
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| Veröffentlicht in: | Experimental brain research 2024-04, Vol.242 (4), p.869-878 |
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| description | Ischemic stroke is one of the most vital causes of high neurological morbidity and mortality in the world. Preconditioning exercise is considered as the primary prevention of stroke to resistance to subsequent injury. We tried to research the underlying biological mechanisms of this exercise. Forty-two SD rats were randomly divided into three groups: middle cerebral artery occlusion (MCAO) group, exercise group with MCAO (EX + MCAO) group, and sham group, with 14 rats in each group. The EX + MCAO group underwent exercise preconditioning for 3 weeks before occlusion, and the other two groups were fed and exercised normally. After 3 weeks, MCAO model was made by thread plug method in the EX + MCAO group and MCAO group. After successful modeling, the Longa scale was used to evaluate the neurological impairment of rats at day 0, day 1, and day 2. The rats in each group were killed on the third day after modeling. TTC staining measured the infarct volume of each group. The morphology and apoptosis of cortical cells were observed by HE and Tunel staining. Three rats in each group underwent high-throughput sequencing. Bioinformatic analysis was used to find the deferentially expressed genes (DEGs) and predict the transcription factor binding sites (TFBS) of the next-generation sequencing results. Gene enrichment (GSEA) was used to analyze potential functional genes and their corresponding signaling pathways. The Longa scale showed EX + MCAO group had the neurological function better than the modeling group (
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| doi_str_mv | 10.1007/s00221-024-06778-y |
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P
< 0.001). TTC staining showed that the infarct size of EX + MCAO group was less than MCAO group (
P
< 0.05). HE and Tunel staining showed that the cells in the EX + MCAO group and the sham group had normal morphology and fewer apoptotic cells than MCAO group. A new gene named 7994 was discovered and TFBS of this gene was predicted, which could interact with key genes such as Foxd3, Foxa2, NR4A2, SP1, CEBPA, and SOX10. GSEA showed that EX + MCAO group could promote and regulate angiogenesis and apoptosis through PI3K–AKT pathway. Preconditioning exercise could improve nerve function and reduce infarct size in rats. The underlying mechanism is to regulate the PI3K–AKT pathway through several key genes, promote cerebral angiogenesis, and reduce apoptosis.</description><identifier>ISSN: 0014-4819</identifier><identifier>EISSN: 1432-1106</identifier><identifier>DOI: 10.1007/s00221-024-06778-y</identifier><identifier>PMID: 38421411</identifier><language>eng</language><publisher>Berlin/Heidelberg: Springer Berlin Heidelberg</publisher><subject>1-Phosphatidylinositol 3-kinase ; AKT protein ; Angiogenesis ; Apoptosis ; Biomedical and Life Sciences ; Biomedicine ; Brain injury ; Cerebral blood flow ; Cytology ; Genes ; Ischemia ; Morbidity ; Morphology ; Neurological complications ; Neurology ; Neurosciences ; Next-generation sequencing ; Research Article ; Sox10 protein ; Stroke</subject><ispartof>Experimental brain research, 2024-04, Vol.242 (4), p.869-878</ispartof><rights>The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature 2024. Springer Nature or its licensor (e.g. a society or other partner) holds exclusive rights to this article under a publishing agreement with the author(s) or other rightsholder(s); author self-archiving of the accepted manuscript version of this article is solely governed by the terms of such publishing agreement and applicable law.</rights><rights>2024. The Author(s), under exclusive licence to Springer-Verlag GmbH Germany, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-3fb4d9c4ce602eeccc51cc6c6b423931ac7a09da4adb523739b3a86ed1b9d833</citedby><cites>FETCH-LOGICAL-c375t-3fb4d9c4ce602eeccc51cc6c6b423931ac7a09da4adb523739b3a86ed1b9d833</cites><orcidid>0000-0002-4834-6954</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><linktopdf>$$Uhttps://link.springer.com/content/pdf/10.1007/s00221-024-06778-y$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s00221-024-06778-y$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,780,784,27923,27924,41487,42556,51318</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/38421411$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Li, Kai</creatorcontrib><creatorcontrib>Gao, Zhen-Kun</creatorcontrib><creatorcontrib>Guo, Yi-Sha</creatorcontrib><creatorcontrib>Shen, Xin-Ya</creatorcontrib><creatorcontrib>Han, Yu</creatorcontrib><creatorcontrib>Yuan, Mei</creatorcontrib><creatorcontrib>Bi, Xia</creatorcontrib><title>Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K–AKT pathway by bioinformatic analysis</title><title>Experimental brain research</title><addtitle>Exp Brain Res</addtitle><addtitle>Exp Brain Res</addtitle><description>Ischemic stroke is one of the most vital causes of high neurological morbidity and mortality in the world. Preconditioning exercise is considered as the primary prevention of stroke to resistance to subsequent injury. We tried to research the underlying biological mechanisms of this exercise. Forty-two SD rats were randomly divided into three groups: middle cerebral artery occlusion (MCAO) group, exercise group with MCAO (EX + MCAO) group, and sham group, with 14 rats in each group. The EX + MCAO group underwent exercise preconditioning for 3 weeks before occlusion, and the other two groups were fed and exercised normally. After 3 weeks, MCAO model was made by thread plug method in the EX + MCAO group and MCAO group. After successful modeling, the Longa scale was used to evaluate the neurological impairment of rats at day 0, day 1, and day 2. The rats in each group were killed on the third day after modeling. TTC staining measured the infarct volume of each group. The morphology and apoptosis of cortical cells were observed by HE and Tunel staining. Three rats in each group underwent high-throughput sequencing. Bioinformatic analysis was used to find the deferentially expressed genes (DEGs) and predict the transcription factor binding sites (TFBS) of the next-generation sequencing results. Gene enrichment (GSEA) was used to analyze potential functional genes and their corresponding signaling pathways. The Longa scale showed EX + MCAO group had the neurological function better than the modeling group (
P
< 0.001). TTC staining showed that the infarct size of EX + MCAO group was less than MCAO group (
P
< 0.05). HE and Tunel staining showed that the cells in the EX + MCAO group and the sham group had normal morphology and fewer apoptotic cells than MCAO group. A new gene named 7994 was discovered and TFBS of this gene was predicted, which could interact with key genes such as Foxd3, Foxa2, NR4A2, SP1, CEBPA, and SOX10. GSEA showed that EX + MCAO group could promote and regulate angiogenesis and apoptosis through PI3K–AKT pathway. Preconditioning exercise could improve nerve function and reduce infarct size in rats. The underlying mechanism is to regulate the PI3K–AKT pathway through several key genes, promote cerebral angiogenesis, and reduce apoptosis.</description><subject>1-Phosphatidylinositol 3-kinase</subject><subject>AKT protein</subject><subject>Angiogenesis</subject><subject>Apoptosis</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain injury</subject><subject>Cerebral blood flow</subject><subject>Cytology</subject><subject>Genes</subject><subject>Ischemia</subject><subject>Morbidity</subject><subject>Morphology</subject><subject>Neurological complications</subject><subject>Neurology</subject><subject>Neurosciences</subject><subject>Next-generation sequencing</subject><subject>Research Article</subject><subject>Sox10 protein</subject><subject>Stroke</subject><issn>0014-4819</issn><issn>1432-1106</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kctu1DAUhi1URKcDL9AFstQNmxTfJpdlVQGtWokuZm-d2CdTt5N48EkK2fEOvCFPgtspILFAsmRZ5_t_2_oYO5biVApRvSchlJKFUKYQZVXVxfyCLaTRqpBSlAdsIYQ0hallc8iOiO4ej7oSr9ihro2SRsoFm28Sujj4MIY4hGHD8RsmFwh5Qj85JN4mCAP30MMGeex4IHeLfXCcxhTvkedhgpH4QwB-c6mvfn7_cXa15jsYb7_CzNu8QgxDF1MPY47BANuZAr1mLzvYEr553pds_fHD-vyiuP786fL87LpwulqNhe5a4xtnHJZCITrnVtK50pWtUbrRElwFovFgwLcrpSvdtBrqEr1sG19rvWTv9rW7FL9MSKPt8w9wu4UB40RWNVqbUprKZPTkH_QuTik_l6wWImOmzP1LpvaUS5EoYWd3KfSQZiuFffRi915s9mKfvNg5h94-V09tj_5P5LeIDOg9QHk0bDD9vfs_tb8Ah-Sbaw</recordid><startdate>20240401</startdate><enddate>20240401</enddate><creator>Li, Kai</creator><creator>Gao, Zhen-Kun</creator><creator>Guo, Yi-Sha</creator><creator>Shen, Xin-Ya</creator><creator>Han, Yu</creator><creator>Yuan, Mei</creator><creator>Bi, Xia</creator><general>Springer Berlin Heidelberg</general><general>Springer Nature B.V</general><scope>NPM</scope><scope>AAYXX</scope><scope>CITATION</scope><scope>7QP</scope><scope>7QR</scope><scope>7TK</scope><scope>7TM</scope><scope>8FD</scope><scope>FR3</scope><scope>K9.</scope><scope>NAPCQ</scope><scope>P64</scope><scope>RC3</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0002-4834-6954</orcidid></search><sort><creationdate>20240401</creationdate><title>Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K–AKT pathway by bioinformatic analysis</title><author>Li, Kai ; Gao, Zhen-Kun ; Guo, Yi-Sha ; Shen, Xin-Ya ; Han, Yu ; Yuan, Mei ; Bi, Xia</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-3fb4d9c4ce602eeccc51cc6c6b423931ac7a09da4adb523739b3a86ed1b9d833</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>1-Phosphatidylinositol 3-kinase</topic><topic>AKT protein</topic><topic>Angiogenesis</topic><topic>Apoptosis</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain injury</topic><topic>Cerebral blood flow</topic><topic>Cytology</topic><topic>Genes</topic><topic>Ischemia</topic><topic>Morbidity</topic><topic>Morphology</topic><topic>Neurological complications</topic><topic>Neurology</topic><topic>Neurosciences</topic><topic>Next-generation sequencing</topic><topic>Research Article</topic><topic>Sox10 protein</topic><topic>Stroke</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Li, Kai</creatorcontrib><creatorcontrib>Gao, Zhen-Kun</creatorcontrib><creatorcontrib>Guo, Yi-Sha</creatorcontrib><creatorcontrib>Shen, Xin-Ya</creatorcontrib><creatorcontrib>Han, Yu</creatorcontrib><creatorcontrib>Yuan, Mei</creatorcontrib><creatorcontrib>Bi, Xia</creatorcontrib><collection>PubMed</collection><collection>CrossRef</collection><collection>Calcium & Calcified Tissue Abstracts</collection><collection>Chemoreception Abstracts</collection><collection>Neurosciences Abstracts</collection><collection>Nucleic Acids Abstracts</collection><collection>Technology Research Database</collection><collection>Engineering Research Database</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>Biotechnology and BioEngineering Abstracts</collection><collection>Genetics Abstracts</collection><collection>MEDLINE - Academic</collection><jtitle>Experimental brain research</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Li, Kai</au><au>Gao, Zhen-Kun</au><au>Guo, Yi-Sha</au><au>Shen, Xin-Ya</au><au>Han, Yu</au><au>Yuan, Mei</au><au>Bi, Xia</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K–AKT pathway by bioinformatic analysis</atitle><jtitle>Experimental brain research</jtitle><stitle>Exp Brain Res</stitle><addtitle>Exp Brain Res</addtitle><date>2024-04-01</date><risdate>2024</risdate><volume>242</volume><issue>4</issue><spage>869</spage><epage>878</epage><pages>869-878</pages><issn>0014-4819</issn><eissn>1432-1106</eissn><abstract>Ischemic stroke is one of the most vital causes of high neurological morbidity and mortality in the world. Preconditioning exercise is considered as the primary prevention of stroke to resistance to subsequent injury. We tried to research the underlying biological mechanisms of this exercise. Forty-two SD rats were randomly divided into three groups: middle cerebral artery occlusion (MCAO) group, exercise group with MCAO (EX + MCAO) group, and sham group, with 14 rats in each group. The EX + MCAO group underwent exercise preconditioning for 3 weeks before occlusion, and the other two groups were fed and exercised normally. After 3 weeks, MCAO model was made by thread plug method in the EX + MCAO group and MCAO group. After successful modeling, the Longa scale was used to evaluate the neurological impairment of rats at day 0, day 1, and day 2. The rats in each group were killed on the third day after modeling. TTC staining measured the infarct volume of each group. The morphology and apoptosis of cortical cells were observed by HE and Tunel staining. Three rats in each group underwent high-throughput sequencing. Bioinformatic analysis was used to find the deferentially expressed genes (DEGs) and predict the transcription factor binding sites (TFBS) of the next-generation sequencing results. Gene enrichment (GSEA) was used to analyze potential functional genes and their corresponding signaling pathways. The Longa scale showed EX + MCAO group had the neurological function better than the modeling group (
P
< 0.001). TTC staining showed that the infarct size of EX + MCAO group was less than MCAO group (
P
< 0.05). HE and Tunel staining showed that the cells in the EX + MCAO group and the sham group had normal morphology and fewer apoptotic cells than MCAO group. A new gene named 7994 was discovered and TFBS of this gene was predicted, which could interact with key genes such as Foxd3, Foxa2, NR4A2, SP1, CEBPA, and SOX10. GSEA showed that EX + MCAO group could promote and regulate angiogenesis and apoptosis through PI3K–AKT pathway. Preconditioning exercise could improve nerve function and reduce infarct size in rats. The underlying mechanism is to regulate the PI3K–AKT pathway through several key genes, promote cerebral angiogenesis, and reduce apoptosis.</abstract><cop>Berlin/Heidelberg</cop><pub>Springer Berlin Heidelberg</pub><pmid>38421411</pmid><doi>10.1007/s00221-024-06778-y</doi><tpages>10</tpages><orcidid>https://orcid.org/0000-0002-4834-6954</orcidid></addata></record> |
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| subjects | 1-Phosphatidylinositol 3-kinase AKT protein Angiogenesis Apoptosis Biomedical and Life Sciences Biomedicine Brain injury Cerebral blood flow Cytology Genes Ischemia Morbidity Morphology Neurological complications Neurology Neurosciences Next-generation sequencing Research Article Sox10 protein Stroke |
| title | Preconditioning exercise reduces brain damage of ischemic stroke in rats via PI3K–AKT pathway by bioinformatic analysis |
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