Nateglinide Exerts Neuroprotective Effects via Downregulation of HIF-1α/TIM-3 Inflammatory Pathway and Promotion of Caveolin-1 Expression in the Rat’s Hippocampus Subjected to Focal Cerebral Ischemia/Reperfusion Injury
Ischemic stroke is a major cause of death and motor disabilities all over the world. It is a muti-factorial disorder associated with inflammatory, apoptotic, and oxidative responses. Nateglinide (NAT), an insulinotropic agent used for the treatment of type 2 diabetes mellitus, recently showed potent...
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| Veröffentlicht in: | Inflammation 2020-04, Vol.43 (2), p.401-416 |
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| creator | Saad, Muhammad Abd El-Latif Fahmy, Mohamed Ibrahim Mohamed Al-Shorbagy, Muhammad Assaf, Naglaa Hegazy, Ahmed Abd El-Aziz El-Yamany, Muhammad Farag |
| description | Ischemic stroke is a major cause of death and motor disabilities all over the world. It is a muti-factorial disorder associated with inflammatory, apoptotic, and oxidative responses. Nateglinide (NAT), an insulinotropic agent used for the treatment of type 2 diabetes mellitus, recently showed potential anti-inflammatory and anti-apoptotic effects. The aim of our study was to elucidate the unique neuroprotective role of NAT in the middle cerebral artery occlusion (MCAO)-induced stroke in rats. Fifty-six male rats were divided to 4 groups (
n
= 14 in each group): the sham-operated group, sham receiving NAT (50 mg/kg/day, p.o) group, ischemia/reperfusion (IR) group, and IR receiving NAT group (50 mg/kg/day, p.o). MCAO caused potent deficits in motor and behavioral functions of the rats. Significant increase in inflammatory and apoptotic biomarkers has been observed in rats’ hippocampi. Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway was significantly stimulated causing activation of series inflammatory biomarkers ending up neuro-inflammatory milieu. Pretreatment with NAT preserved rats’ normal behavioral and motor functions. Moreover, NAT opposed the expression of hypoxia-inducible factor-1α (HIF-1α) resulting in downregulation of more inflammatory mediators namely, NF-κB, tumor necrosis factor-β (TNF-β), and the anti-survival gene PMAIP-1. NAT stimulated caveolin-1 (Cav-1) which prevented expression of oxidative biomarkers, nitric oxide (NO), and myeloperoxidase (MPO) and hamper the activation of apoptotic biomarker caspase-3. In conclusion, our work postulated that NAT exhibited its neuroprotective effects in rats with ischemic stroke
via
attenuation of different unique oxidative, apoptotic, and inflammatory pathways. |
| doi_str_mv | 10.1007/s10753-019-01154-3 |
| format | Article |
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n
= 14 in each group): the sham-operated group, sham receiving NAT (50 mg/kg/day, p.o) group, ischemia/reperfusion (IR) group, and IR receiving NAT group (50 mg/kg/day, p.o). MCAO caused potent deficits in motor and behavioral functions of the rats. Significant increase in inflammatory and apoptotic biomarkers has been observed in rats’ hippocampi. Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway was significantly stimulated causing activation of series inflammatory biomarkers ending up neuro-inflammatory milieu. Pretreatment with NAT preserved rats’ normal behavioral and motor functions. Moreover, NAT opposed the expression of hypoxia-inducible factor-1α (HIF-1α) resulting in downregulation of more inflammatory mediators namely, NF-κB, tumor necrosis factor-β (TNF-β), and the anti-survival gene PMAIP-1. NAT stimulated caveolin-1 (Cav-1) which prevented expression of oxidative biomarkers, nitric oxide (NO), and myeloperoxidase (MPO) and hamper the activation of apoptotic biomarker caspase-3. In conclusion, our work postulated that NAT exhibited its neuroprotective effects in rats with ischemic stroke
via
attenuation of different unique oxidative, apoptotic, and inflammatory pathways.</description><identifier>ISSN: 0360-3997</identifier><identifier>EISSN: 1573-2576</identifier><identifier>DOI: 10.1007/s10753-019-01154-3</identifier><identifier>PMID: 31863220</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Animals ; Apoptosis ; Biomarkers ; Biomedical and Life Sciences ; Biomedicine ; Brain Ischemia - metabolism ; Brain Ischemia - pathology ; Brain Ischemia - prevention & control ; Caspase-3 ; Caveolin ; Caveolin 1 - biosynthesis ; Caveolin-1 ; Cerebral blood flow ; Diabetes mellitus (non-insulin dependent) ; Down-Regulation - drug effects ; Down-Regulation - physiology ; Hippocampus ; Hippocampus - drug effects ; Hippocampus - metabolism ; Hippocampus - pathology ; Hypoxia-Inducible Factor 1, alpha Subunit - antagonists & inhibitors ; Hypoxia-Inducible Factor 1, alpha Subunit - metabolism ; Hypoxia-inducible factors ; Immunology ; Inflammation Mediators - antagonists & inhibitors ; Inflammation Mediators - metabolism ; Internal Medicine ; Ischemia ; Janus kinase ; Janus kinase 2 ; Male ; Nateglinide - pharmacology ; Nateglinide - therapeutic use ; Neuroprotection ; Neuroprotective Agents - pharmacology ; Neuroprotective Agents - therapeutic use ; NF-κB protein ; Nitric oxide ; Original Article ; Pathology ; Peroxidase ; Pharmacology/Toxicology ; Psychomotor Performance - drug effects ; Psychomotor Performance - physiology ; Rats ; Rats, Wistar ; Receptors, Cell Surface - antagonists & inhibitors ; Receptors, Cell Surface - metabolism ; Reperfusion ; Reperfusion Injury - metabolism ; Reperfusion Injury - pathology ; Reperfusion Injury - prevention & control ; Rheumatology ; Rodents ; Signal Transduction - drug effects ; Signal Transduction - physiology ; Stat3 protein ; Stroke ; Transcription ; Tumor necrosis factor ; Tumor necrosis factor-TNF</subject><ispartof>Inflammation, 2020-04, Vol.43 (2), p.401-416</ispartof><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019</rights><rights>Springer Science+Business Media, LLC, part of Springer Nature 2019.</rights><lds50>peer_reviewed</lds50><oa>free_for_read</oa><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c419t-a90fbaac4a012b499bba6e53f1dd8df9f4bdb11fb7f5a01fc5a4adefb070efc43</citedby><cites>FETCH-LOGICAL-c419t-a90fbaac4a012b499bba6e53f1dd8df9f4bdb11fb7f5a01fc5a4adefb070efc43</cites><orcidid>0000-0003-3660-3981</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/s10753-019-01154-3$$EPDF$$P50$$Gspringer$$H</linktopdf><linktohtml>$$Uhttps://link.springer.com/10.1007/s10753-019-01154-3$$EHTML$$P50$$Gspringer$$H</linktohtml><link.rule.ids>314,776,780,27903,27904,41467,42536,51297</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/31863220$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Saad, Muhammad Abd El-Latif</creatorcontrib><creatorcontrib>Fahmy, Mohamed Ibrahim Mohamed</creatorcontrib><creatorcontrib>Al-Shorbagy, Muhammad</creatorcontrib><creatorcontrib>Assaf, Naglaa</creatorcontrib><creatorcontrib>Hegazy, Ahmed Abd El-Aziz</creatorcontrib><creatorcontrib>El-Yamany, Muhammad Farag</creatorcontrib><title>Nateglinide Exerts Neuroprotective Effects via Downregulation of HIF-1α/TIM-3 Inflammatory Pathway and Promotion of Caveolin-1 Expression in the Rat’s Hippocampus Subjected to Focal Cerebral Ischemia/Reperfusion Injury</title><title>Inflammation</title><addtitle>Inflammation</addtitle><addtitle>Inflammation</addtitle><description>Ischemic stroke is a major cause of death and motor disabilities all over the world. It is a muti-factorial disorder associated with inflammatory, apoptotic, and oxidative responses. Nateglinide (NAT), an insulinotropic agent used for the treatment of type 2 diabetes mellitus, recently showed potential anti-inflammatory and anti-apoptotic effects. The aim of our study was to elucidate the unique neuroprotective role of NAT in the middle cerebral artery occlusion (MCAO)-induced stroke in rats. Fifty-six male rats were divided to 4 groups (
n
= 14 in each group): the sham-operated group, sham receiving NAT (50 mg/kg/day, p.o) group, ischemia/reperfusion (IR) group, and IR receiving NAT group (50 mg/kg/day, p.o). MCAO caused potent deficits in motor and behavioral functions of the rats. Significant increase in inflammatory and apoptotic biomarkers has been observed in rats’ hippocampi. Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway was significantly stimulated causing activation of series inflammatory biomarkers ending up neuro-inflammatory milieu. Pretreatment with NAT preserved rats’ normal behavioral and motor functions. Moreover, NAT opposed the expression of hypoxia-inducible factor-1α (HIF-1α) resulting in downregulation of more inflammatory mediators namely, NF-κB, tumor necrosis factor-β (TNF-β), and the anti-survival gene PMAIP-1. NAT stimulated caveolin-1 (Cav-1) which prevented expression of oxidative biomarkers, nitric oxide (NO), and myeloperoxidase (MPO) and hamper the activation of apoptotic biomarker caspase-3. In conclusion, our work postulated that NAT exhibited its neuroprotective effects in rats with ischemic stroke
via
attenuation of different unique oxidative, apoptotic, and inflammatory pathways.</description><subject>Animals</subject><subject>Apoptosis</subject><subject>Biomarkers</subject><subject>Biomedical and Life Sciences</subject><subject>Biomedicine</subject><subject>Brain Ischemia - metabolism</subject><subject>Brain Ischemia - pathology</subject><subject>Brain Ischemia - prevention & control</subject><subject>Caspase-3</subject><subject>Caveolin</subject><subject>Caveolin 1 - biosynthesis</subject><subject>Caveolin-1</subject><subject>Cerebral blood flow</subject><subject>Diabetes mellitus (non-insulin dependent)</subject><subject>Down-Regulation - drug effects</subject><subject>Down-Regulation - physiology</subject><subject>Hippocampus</subject><subject>Hippocampus - drug effects</subject><subject>Hippocampus - metabolism</subject><subject>Hippocampus - pathology</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - antagonists & inhibitors</subject><subject>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</subject><subject>Hypoxia-inducible factors</subject><subject>Immunology</subject><subject>Inflammation Mediators - antagonists & inhibitors</subject><subject>Inflammation Mediators - metabolism</subject><subject>Internal Medicine</subject><subject>Ischemia</subject><subject>Janus kinase</subject><subject>Janus kinase 2</subject><subject>Male</subject><subject>Nateglinide - pharmacology</subject><subject>Nateglinide - therapeutic use</subject><subject>Neuroprotection</subject><subject>Neuroprotective Agents - pharmacology</subject><subject>Neuroprotective Agents - therapeutic use</subject><subject>NF-κB protein</subject><subject>Nitric oxide</subject><subject>Original Article</subject><subject>Pathology</subject><subject>Peroxidase</subject><subject>Pharmacology/Toxicology</subject><subject>Psychomotor Performance - drug effects</subject><subject>Psychomotor Performance - physiology</subject><subject>Rats</subject><subject>Rats, Wistar</subject><subject>Receptors, Cell Surface - antagonists & inhibitors</subject><subject>Receptors, Cell Surface - metabolism</subject><subject>Reperfusion</subject><subject>Reperfusion Injury - metabolism</subject><subject>Reperfusion Injury - pathology</subject><subject>Reperfusion Injury - prevention & control</subject><subject>Rheumatology</subject><subject>Rodents</subject><subject>Signal Transduction - drug effects</subject><subject>Signal Transduction - physiology</subject><subject>Stat3 protein</subject><subject>Stroke</subject><subject>Transcription</subject><subject>Tumor necrosis factor</subject><subject>Tumor necrosis factor-TNF</subject><issn>0360-3997</issn><issn>1573-2576</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2020</creationdate><recordtype>article</recordtype><sourceid>EIF</sourceid><sourceid>ABUWG</sourceid><sourceid>AFKRA</sourceid><sourceid>BENPR</sourceid><sourceid>CCPQU</sourceid><recordid>eNp9Uc1u1DAQthCILoUX4IAscTZrx8kmPqKly0YqpSrlHI2T8W5WSRxsZ8veeA0egxfhDbjwJLjdFm4cRjOa-X4sf4S8FPyN4Dyfe8HzTDIuVCyRpUw-IjOR5ZIlWb54TGZcLjiTSuUn5Jn3O855oQr5lJxIUSxkkvAZ-XUBATddO7QN0rOv6IKnFzg5OzobsA7tPq6NiZOn-xboO3szONxMHYTWDtQaui5XTPz8Mb8uPzBJy8F00PcQrDvQSwjbGzhQGBp66WxvHzhL2KONpkxEz9Gh97eHdqBhi_QKwu9v3z1dt-Noa-jHydNPk97FN2BDg6WruO3oEh1qF4fS11vsW5hf4YjOTHda5bCb3OE5eWKg8_jivp-Sz6uz6-WanX98Xy7fnrM6FSowUNxogDoFLhKdKqU1LDCTRjRN0RhlUt1oIYzOTRYhps4ghQaN5jlHU6fylLw-6sZf-zKhD9XOTm6IllUiVZKoIk14RCVHVO2s9w5NNbq2B3eoBK9uE62OiVYx0eou0UpG0qt76Un32PylPEQYAfII8PE0bND98_6P7B-RZrOR</recordid><startdate>20200401</startdate><enddate>20200401</enddate><creator>Saad, Muhammad Abd El-Latif</creator><creator>Fahmy, Mohamed Ibrahim Mohamed</creator><creator>Al-Shorbagy, Muhammad</creator><creator>Assaf, Naglaa</creator><creator>Hegazy, Ahmed Abd El-Aziz</creator><creator>El-Yamany, Muhammad Farag</creator><general>Springer US</general><general>Springer Nature 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>3V.</scope><scope>7T5</scope><scope>7TO</scope><scope>7U9</scope><scope>7X7</scope><scope>7XB</scope><scope>88E</scope><scope>8AO</scope><scope>8FI</scope><scope>8FJ</scope><scope>8FK</scope><scope>ABUWG</scope><scope>AFKRA</scope><scope>BENPR</scope><scope>CCPQU</scope><scope>FYUFA</scope><scope>GHDGH</scope><scope>H94</scope><scope>K9.</scope><scope>M0S</scope><scope>M1P</scope><scope>PQEST</scope><scope>PQQKQ</scope><scope>PQUKI</scope><scope>PRINS</scope><orcidid>https://orcid.org/0000-0003-3660-3981</orcidid></search><sort><creationdate>20200401</creationdate><title>Nateglinide Exerts Neuroprotective Effects via Downregulation of HIF-1α/TIM-3 Inflammatory Pathway and Promotion of Caveolin-1 Expression in the Rat’s Hippocampus Subjected to Focal Cerebral Ischemia/Reperfusion Injury</title><author>Saad, Muhammad Abd El-Latif ; Fahmy, Mohamed Ibrahim Mohamed ; Al-Shorbagy, Muhammad ; Assaf, Naglaa ; Hegazy, Ahmed Abd El-Aziz ; El-Yamany, Muhammad Farag</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c419t-a90fbaac4a012b499bba6e53f1dd8df9f4bdb11fb7f5a01fc5a4adefb070efc43</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2020</creationdate><topic>Animals</topic><topic>Apoptosis</topic><topic>Biomarkers</topic><topic>Biomedical and Life Sciences</topic><topic>Biomedicine</topic><topic>Brain Ischemia - metabolism</topic><topic>Brain Ischemia - pathology</topic><topic>Brain Ischemia - prevention & control</topic><topic>Caspase-3</topic><topic>Caveolin</topic><topic>Caveolin 1 - biosynthesis</topic><topic>Caveolin-1</topic><topic>Cerebral blood flow</topic><topic>Diabetes mellitus (non-insulin dependent)</topic><topic>Down-Regulation - drug effects</topic><topic>Down-Regulation - physiology</topic><topic>Hippocampus</topic><topic>Hippocampus - drug effects</topic><topic>Hippocampus - metabolism</topic><topic>Hippocampus - pathology</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - antagonists & inhibitors</topic><topic>Hypoxia-Inducible Factor 1, alpha Subunit - metabolism</topic><topic>Hypoxia-inducible factors</topic><topic>Immunology</topic><topic>Inflammation Mediators - antagonists & inhibitors</topic><topic>Inflammation Mediators - metabolism</topic><topic>Internal Medicine</topic><topic>Ischemia</topic><topic>Janus kinase</topic><topic>Janus kinase 2</topic><topic>Male</topic><topic>Nateglinide - pharmacology</topic><topic>Nateglinide - therapeutic use</topic><topic>Neuroprotection</topic><topic>Neuroprotective Agents - pharmacology</topic><topic>Neuroprotective Agents - therapeutic use</topic><topic>NF-κB protein</topic><topic>Nitric oxide</topic><topic>Original Article</topic><topic>Pathology</topic><topic>Peroxidase</topic><topic>Pharmacology/Toxicology</topic><topic>Psychomotor Performance - drug effects</topic><topic>Psychomotor Performance - physiology</topic><topic>Rats</topic><topic>Rats, Wistar</topic><topic>Receptors, Cell Surface - antagonists & inhibitors</topic><topic>Receptors, Cell Surface - metabolism</topic><topic>Reperfusion</topic><topic>Reperfusion Injury - metabolism</topic><topic>Reperfusion Injury - pathology</topic><topic>Reperfusion Injury - prevention & control</topic><topic>Rheumatology</topic><topic>Rodents</topic><topic>Signal Transduction - drug effects</topic><topic>Signal Transduction - physiology</topic><topic>Stat3 protein</topic><topic>Stroke</topic><topic>Transcription</topic><topic>Tumor necrosis factor</topic><topic>Tumor necrosis factor-TNF</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Saad, Muhammad Abd El-Latif</creatorcontrib><creatorcontrib>Fahmy, Mohamed Ibrahim Mohamed</creatorcontrib><creatorcontrib>Al-Shorbagy, Muhammad</creatorcontrib><creatorcontrib>Assaf, Naglaa</creatorcontrib><creatorcontrib>Hegazy, Ahmed Abd El-Aziz</creatorcontrib><creatorcontrib>El-Yamany, Muhammad Farag</creatorcontrib><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>CrossRef</collection><collection>ProQuest Central (Corporate)</collection><collection>Immunology Abstracts</collection><collection>Oncogenes and Growth Factors Abstracts</collection><collection>Virology and AIDS Abstracts</collection><collection>Health & Medical Collection</collection><collection>ProQuest Central (purchase pre-March 2016)</collection><collection>Medical Database (Alumni Edition)</collection><collection>ProQuest Pharma Collection</collection><collection>Hospital Premium Collection</collection><collection>Hospital Premium Collection (Alumni Edition)</collection><collection>ProQuest Central (Alumni) (purchase pre-March 2016)</collection><collection>ProQuest Central (Alumni Edition)</collection><collection>ProQuest Central UK/Ireland</collection><collection>ProQuest Central</collection><collection>ProQuest One Community College</collection><collection>Health Research Premium Collection</collection><collection>Health Research Premium Collection (Alumni)</collection><collection>AIDS and Cancer Research Abstracts</collection><collection>ProQuest Health & Medical Complete (Alumni)</collection><collection>Health & Medical Collection (Alumni Edition)</collection><collection>Medical Database</collection><collection>ProQuest One Academic Eastern Edition (DO NOT USE)</collection><collection>ProQuest One Academic</collection><collection>ProQuest One Academic UKI Edition</collection><collection>ProQuest Central China</collection><jtitle>Inflammation</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Saad, Muhammad Abd El-Latif</au><au>Fahmy, Mohamed Ibrahim Mohamed</au><au>Al-Shorbagy, Muhammad</au><au>Assaf, Naglaa</au><au>Hegazy, Ahmed Abd El-Aziz</au><au>El-Yamany, Muhammad Farag</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Nateglinide Exerts Neuroprotective Effects via Downregulation of HIF-1α/TIM-3 Inflammatory Pathway and Promotion of Caveolin-1 Expression in the Rat’s Hippocampus Subjected to Focal Cerebral Ischemia/Reperfusion Injury</atitle><jtitle>Inflammation</jtitle><stitle>Inflammation</stitle><addtitle>Inflammation</addtitle><date>2020-04-01</date><risdate>2020</risdate><volume>43</volume><issue>2</issue><spage>401</spage><epage>416</epage><pages>401-416</pages><issn>0360-3997</issn><eissn>1573-2576</eissn><abstract>Ischemic stroke is a major cause of death and motor disabilities all over the world. It is a muti-factorial disorder associated with inflammatory, apoptotic, and oxidative responses. Nateglinide (NAT), an insulinotropic agent used for the treatment of type 2 diabetes mellitus, recently showed potential anti-inflammatory and anti-apoptotic effects. The aim of our study was to elucidate the unique neuroprotective role of NAT in the middle cerebral artery occlusion (MCAO)-induced stroke in rats. Fifty-six male rats were divided to 4 groups (
n
= 14 in each group): the sham-operated group, sham receiving NAT (50 mg/kg/day, p.o) group, ischemia/reperfusion (IR) group, and IR receiving NAT group (50 mg/kg/day, p.o). MCAO caused potent deficits in motor and behavioral functions of the rats. Significant increase in inflammatory and apoptotic biomarkers has been observed in rats’ hippocampi. Janus kinase 2 (JAK2)/signal transducer and activator of transcription 3 (STAT3) pathway was significantly stimulated causing activation of series inflammatory biomarkers ending up neuro-inflammatory milieu. Pretreatment with NAT preserved rats’ normal behavioral and motor functions. Moreover, NAT opposed the expression of hypoxia-inducible factor-1α (HIF-1α) resulting in downregulation of more inflammatory mediators namely, NF-κB, tumor necrosis factor-β (TNF-β), and the anti-survival gene PMAIP-1. NAT stimulated caveolin-1 (Cav-1) which prevented expression of oxidative biomarkers, nitric oxide (NO), and myeloperoxidase (MPO) and hamper the activation of apoptotic biomarker caspase-3. In conclusion, our work postulated that NAT exhibited its neuroprotective effects in rats with ischemic stroke
via
attenuation of different unique oxidative, apoptotic, and inflammatory pathways.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>31863220</pmid><doi>10.1007/s10753-019-01154-3</doi><tpages>16</tpages><orcidid>https://orcid.org/0000-0003-3660-3981</orcidid><oa>free_for_read</oa></addata></record> |
| fulltext | fulltext |
| identifier | ISSN: 0360-3997 |
| ispartof | Inflammation, 2020-04, Vol.43 (2), p.401-416 |
| issn | 0360-3997 1573-2576 |
| language | eng |
| recordid | cdi_proquest_journals_2392298420 |
| source | MEDLINE; Springer Nature - Complete Springer Journals |
| subjects | Animals Apoptosis Biomarkers Biomedical and Life Sciences Biomedicine Brain Ischemia - metabolism Brain Ischemia - pathology Brain Ischemia - prevention & control Caspase-3 Caveolin Caveolin 1 - biosynthesis Caveolin-1 Cerebral blood flow Diabetes mellitus (non-insulin dependent) Down-Regulation - drug effects Down-Regulation - physiology Hippocampus Hippocampus - drug effects Hippocampus - metabolism Hippocampus - pathology Hypoxia-Inducible Factor 1, alpha Subunit - antagonists & inhibitors Hypoxia-Inducible Factor 1, alpha Subunit - metabolism Hypoxia-inducible factors Immunology Inflammation Mediators - antagonists & inhibitors Inflammation Mediators - metabolism Internal Medicine Ischemia Janus kinase Janus kinase 2 Male Nateglinide - pharmacology Nateglinide - therapeutic use Neuroprotection Neuroprotective Agents - pharmacology Neuroprotective Agents - therapeutic use NF-κB protein Nitric oxide Original Article Pathology Peroxidase Pharmacology/Toxicology Psychomotor Performance - drug effects Psychomotor Performance - physiology Rats Rats, Wistar Receptors, Cell Surface - antagonists & inhibitors Receptors, Cell Surface - metabolism Reperfusion Reperfusion Injury - metabolism Reperfusion Injury - pathology Reperfusion Injury - prevention & control Rheumatology Rodents Signal Transduction - drug effects Signal Transduction - physiology Stat3 protein Stroke Transcription Tumor necrosis factor Tumor necrosis factor-TNF |
| title | Nateglinide Exerts Neuroprotective Effects via Downregulation of HIF-1α/TIM-3 Inflammatory Pathway and Promotion of Caveolin-1 Expression in the Rat’s Hippocampus Subjected to Focal Cerebral Ischemia/Reperfusion Injury |
| url | https://sfx.bib-bvb.de/sfx_tum?ctx_ver=Z39.88-2004&ctx_enc=info:ofi/enc:UTF-8&ctx_tim=2025-01-23T23%3A24%3A33IST&url_ver=Z39.88-2004&url_ctx_fmt=infofi/fmt:kev:mtx:ctx&rfr_id=info:sid/primo.exlibrisgroup.com:primo3-Article-proquest_cross&rft_val_fmt=info:ofi/fmt:kev:mtx:journal&rft.genre=article&rft.atitle=Nateglinide%20Exerts%20Neuroprotective%20Effects%20via%20Downregulation%20of%20HIF-1%CE%B1/TIM-3%20Inflammatory%20Pathway%20and%20Promotion%20of%20Caveolin-1%20Expression%20in%20the%20Rat%E2%80%99s%20Hippocampus%20Subjected%20to%20Focal%20Cerebral%20Ischemia/Reperfusion%20Injury&rft.jtitle=Inflammation&rft.au=Saad,%20Muhammad%20Abd%20El-Latif&rft.date=2020-04-01&rft.volume=43&rft.issue=2&rft.spage=401&rft.epage=416&rft.pages=401-416&rft.issn=0360-3997&rft.eissn=1573-2576&rft_id=info:doi/10.1007/s10753-019-01154-3&rft_dat=%3Cproquest_cross%3E2392298420%3C/proquest_cross%3E%3Curl%3E%3C/url%3E&disable_directlink=true&sfx.directlink=off&sfx.report_link=0&rft_id=info:oai/&rft_pqid=2392298420&rft_id=info:pmid/31863220&rfr_iscdi=true |