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Hippocampal Microglia Activation Induced by Acute Pancreatic Injury in Rats
Background Acute pancreatitis is an inflammation of the pancreatic glandular parenchyma that causes injury with or without the destruction of pancreatic acini. Clinical and experimental evidence suggest that certain systemic proinflammatory mediators may be responsible for initiating the fundamental...
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Published in: | Digestive diseases and sciences 2024, Vol.69 (1), p.148-160 |
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creator | Cabral-França, Tamires Cruz, Fernanda Ferreira Silva, Paulo Cesar Pannain, Vera Lucia Nunes Fernandes, Arlete Eulálio, José Marcus Raso Paiva, Maurício Magalhães Macedo-Ramos, Hugo Manso, Jose Eduardo Ferreira Baetas-da-Cruz, Wagner |
description | Background
Acute pancreatitis is an inflammation of the pancreatic glandular parenchyma that causes injury with or without the destruction of pancreatic acini. Clinical and experimental evidence suggest that certain systemic proinflammatory mediators may be responsible for initiating the fundamental mechanisms involved in microglial reactivity. Here, we investigated the possible repercussions of acute pancreatitis (AP) on the production of inflammatory mediators in the brain parenchyma focusing on microglial activation in the hippocampus.
Methods
The acute pancreatic injury in rats was induced by a pancreas ligation surgical procedure (PLSP) on the splenic lobe, which corresponds to approximately 10% of total mass of the pancreas. Blood samples were collected via intracardiac puncture for the measurement of serum amylase. After euthanasia, frozen or paraffin-embedded brains and pancreas were analyzed using qRT-PCR or immunohistochemistry, respectively.
Results
Immunohistochemistry assays showed a large number of Iba1 and PU.1-positive cells in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus of the PLSP group. TNF-α mRNA expression was significantly higher in the brain from PLSP group. NLRP3 inflammasome expression was found to be significantly increased in the pancreas and brain of rats of the PLSP group. High levels of BNDF mRNA were found in the rat brain of PLSP group. In contrast, NGF mRNA levels were significantly higher in the control group versus PLSP group.
Conclusion
Our findings suggest that AP has the potential to induce morphological changes in microglia consistent with an activated phenotype. |
doi_str_mv | 10.1007/s10620-023-08167-x |
format | article |
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Acute pancreatitis is an inflammation of the pancreatic glandular parenchyma that causes injury with or without the destruction of pancreatic acini. Clinical and experimental evidence suggest that certain systemic proinflammatory mediators may be responsible for initiating the fundamental mechanisms involved in microglial reactivity. Here, we investigated the possible repercussions of acute pancreatitis (AP) on the production of inflammatory mediators in the brain parenchyma focusing on microglial activation in the hippocampus.
Methods
The acute pancreatic injury in rats was induced by a pancreas ligation surgical procedure (PLSP) on the splenic lobe, which corresponds to approximately 10% of total mass of the pancreas. Blood samples were collected via intracardiac puncture for the measurement of serum amylase. After euthanasia, frozen or paraffin-embedded brains and pancreas were analyzed using qRT-PCR or immunohistochemistry, respectively.
Results
Immunohistochemistry assays showed a large number of Iba1 and PU.1-positive cells in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus of the PLSP group. TNF-α mRNA expression was significantly higher in the brain from PLSP group. NLRP3 inflammasome expression was found to be significantly increased in the pancreas and brain of rats of the PLSP group. High levels of BNDF mRNA were found in the rat brain of PLSP group. In contrast, NGF mRNA levels were significantly higher in the control group versus PLSP group.
Conclusion
Our findings suggest that AP has the potential to induce morphological changes in microglia consistent with an activated phenotype.</description><identifier>ISSN: 0163-2116</identifier><identifier>EISSN: 1573-2568</identifier><identifier>DOI: 10.1007/s10620-023-08167-x</identifier><identifier>PMID: 37957410</identifier><language>eng</language><publisher>New York: Springer US</publisher><subject>Acute Disease ; Animals ; Biochemistry ; Brain ; Gastroenterology ; Hepatology ; Hippocampus - metabolism ; Medicine ; Medicine & Public Health ; Microglia - metabolism ; Oncology ; Original Article ; Pancreas ; Pancreas - metabolism ; Pancreatitis ; Pancreatitis - metabolism ; Rats ; RNA, Messenger - metabolism ; Transplant Surgery</subject><ispartof>Digestive diseases and sciences, 2024, Vol.69 (1), p.148-160</ispartof><rights>The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature 2023. 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>2023. The Author(s), under exclusive licence to Springer Science+Business Media, LLC, part of Springer Nature.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c375t-c18a27af7bae714675df2d89a80a1169d1cf175d8c088dd7dc83ab34c3f9d513</citedby><cites>FETCH-LOGICAL-c375t-c18a27af7bae714675df2d89a80a1169d1cf175d8c088dd7dc83ab34c3f9d513</cites><orcidid>0000-0001-7847-022X</orcidid></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>314,780,784,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/37957410$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink></links><search><creatorcontrib>Cabral-França, Tamires</creatorcontrib><creatorcontrib>Cruz, Fernanda Ferreira</creatorcontrib><creatorcontrib>Silva, Paulo Cesar</creatorcontrib><creatorcontrib>Pannain, Vera Lucia Nunes</creatorcontrib><creatorcontrib>Fernandes, Arlete</creatorcontrib><creatorcontrib>Eulálio, José Marcus Raso</creatorcontrib><creatorcontrib>Paiva, Maurício Magalhães</creatorcontrib><creatorcontrib>Macedo-Ramos, Hugo</creatorcontrib><creatorcontrib>Manso, Jose Eduardo Ferreira</creatorcontrib><creatorcontrib>Baetas-da-Cruz, Wagner</creatorcontrib><title>Hippocampal Microglia Activation Induced by Acute Pancreatic Injury in Rats</title><title>Digestive diseases and sciences</title><addtitle>Dig Dis Sci</addtitle><addtitle>Dig Dis Sci</addtitle><description>Background
Acute pancreatitis is an inflammation of the pancreatic glandular parenchyma that causes injury with or without the destruction of pancreatic acini. Clinical and experimental evidence suggest that certain systemic proinflammatory mediators may be responsible for initiating the fundamental mechanisms involved in microglial reactivity. Here, we investigated the possible repercussions of acute pancreatitis (AP) on the production of inflammatory mediators in the brain parenchyma focusing on microglial activation in the hippocampus.
Methods
The acute pancreatic injury in rats was induced by a pancreas ligation surgical procedure (PLSP) on the splenic lobe, which corresponds to approximately 10% of total mass of the pancreas. Blood samples were collected via intracardiac puncture for the measurement of serum amylase. After euthanasia, frozen or paraffin-embedded brains and pancreas were analyzed using qRT-PCR or immunohistochemistry, respectively.
Results
Immunohistochemistry assays showed a large number of Iba1 and PU.1-positive cells in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus of the PLSP group. TNF-α mRNA expression was significantly higher in the brain from PLSP group. NLRP3 inflammasome expression was found to be significantly increased in the pancreas and brain of rats of the PLSP group. High levels of BNDF mRNA were found in the rat brain of PLSP group. In contrast, NGF mRNA levels were significantly higher in the control group versus PLSP group.
Conclusion
Our findings suggest that AP has the potential to induce morphological changes in microglia consistent with an activated phenotype.</description><subject>Acute Disease</subject><subject>Animals</subject><subject>Biochemistry</subject><subject>Brain</subject><subject>Gastroenterology</subject><subject>Hepatology</subject><subject>Hippocampus - metabolism</subject><subject>Medicine</subject><subject>Medicine & Public Health</subject><subject>Microglia - metabolism</subject><subject>Oncology</subject><subject>Original Article</subject><subject>Pancreas</subject><subject>Pancreas - metabolism</subject><subject>Pancreatitis</subject><subject>Pancreatitis - metabolism</subject><subject>Rats</subject><subject>RNA, Messenger - metabolism</subject><subject>Transplant Surgery</subject><issn>0163-2116</issn><issn>1573-2568</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2024</creationdate><recordtype>article</recordtype><recordid>eNp9kMFPwyAYxYnRuDn9BzyYJl68VPlgLXBcFnWLMxqzO6FAly5dW6E1238vs1MTD54g3_t9j8dD6BLwLWDM7jzglOAYExpjDimLt0doCAmjMUlSfoyGGNJwB0gH6Mz7NcZYMEhP0YAykbAx4CF6mhVNU2u1aVQZPRfa1auyUNFEt8WHaou6iuaV6bQ1UbYL06610auqtLNB1EFbd24XFVX0plp_jk5yVXp7cThHaPlwv5zO4sXL43w6WcSasqSNNXBFmMpZpiyDccoSkxPDheJYhazCgM4hDLnGnBvDjOZUZXSsaS5MAnSEbnrbxtXvnfWt3BRe27JUla07LwnnQgjGUhzQ6z_ouu5cFcJJIiCkIYLvKdJT4ffeO5vLxhUb5XYSsNw3LfumZWhafjUtt2Hp6mDdZRtrfla-qw0A7QEfpGpl3e_b_9h-AsFKiOc</recordid><startdate>2024</startdate><enddate>2024</enddate><creator>Cabral-França, Tamires</creator><creator>Cruz, Fernanda Ferreira</creator><creator>Silva, Paulo Cesar</creator><creator>Pannain, Vera Lucia Nunes</creator><creator>Fernandes, Arlete</creator><creator>Eulálio, José Marcus Raso</creator><creator>Paiva, Maurício Magalhães</creator><creator>Macedo-Ramos, Hugo</creator><creator>Manso, Jose Eduardo Ferreira</creator><creator>Baetas-da-Cruz, Wagner</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>K9.</scope><scope>NAPCQ</scope><scope>7X8</scope><orcidid>https://orcid.org/0000-0001-7847-022X</orcidid></search><sort><creationdate>2024</creationdate><title>Hippocampal Microglia Activation Induced by Acute Pancreatic Injury in Rats</title><author>Cabral-França, Tamires ; Cruz, Fernanda Ferreira ; Silva, Paulo Cesar ; Pannain, Vera Lucia Nunes ; Fernandes, Arlete ; Eulálio, José Marcus Raso ; Paiva, Maurício Magalhães ; Macedo-Ramos, Hugo ; Manso, Jose Eduardo Ferreira ; Baetas-da-Cruz, Wagner</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c375t-c18a27af7bae714675df2d89a80a1169d1cf175d8c088dd7dc83ab34c3f9d513</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2024</creationdate><topic>Acute Disease</topic><topic>Animals</topic><topic>Biochemistry</topic><topic>Brain</topic><topic>Gastroenterology</topic><topic>Hepatology</topic><topic>Hippocampus - metabolism</topic><topic>Medicine</topic><topic>Medicine & Public Health</topic><topic>Microglia - metabolism</topic><topic>Oncology</topic><topic>Original Article</topic><topic>Pancreas</topic><topic>Pancreas - metabolism</topic><topic>Pancreatitis</topic><topic>Pancreatitis - metabolism</topic><topic>Rats</topic><topic>RNA, Messenger - metabolism</topic><topic>Transplant Surgery</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Cabral-França, Tamires</creatorcontrib><creatorcontrib>Cruz, Fernanda Ferreira</creatorcontrib><creatorcontrib>Silva, Paulo Cesar</creatorcontrib><creatorcontrib>Pannain, Vera Lucia Nunes</creatorcontrib><creatorcontrib>Fernandes, Arlete</creatorcontrib><creatorcontrib>Eulálio, José Marcus Raso</creatorcontrib><creatorcontrib>Paiva, Maurício Magalhães</creatorcontrib><creatorcontrib>Macedo-Ramos, Hugo</creatorcontrib><creatorcontrib>Manso, Jose Eduardo Ferreira</creatorcontrib><creatorcontrib>Baetas-da-Cruz, Wagner</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 Health & Medical Complete (Alumni)</collection><collection>Nursing & Allied Health Premium</collection><collection>MEDLINE - Academic</collection><jtitle>Digestive diseases and sciences</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Cabral-França, Tamires</au><au>Cruz, Fernanda Ferreira</au><au>Silva, Paulo Cesar</au><au>Pannain, Vera Lucia Nunes</au><au>Fernandes, Arlete</au><au>Eulálio, José Marcus Raso</au><au>Paiva, Maurício Magalhães</au><au>Macedo-Ramos, Hugo</au><au>Manso, Jose Eduardo Ferreira</au><au>Baetas-da-Cruz, Wagner</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Hippocampal Microglia Activation Induced by Acute Pancreatic Injury in Rats</atitle><jtitle>Digestive diseases and sciences</jtitle><stitle>Dig Dis Sci</stitle><addtitle>Dig Dis Sci</addtitle><date>2024</date><risdate>2024</risdate><volume>69</volume><issue>1</issue><spage>148</spage><epage>160</epage><pages>148-160</pages><issn>0163-2116</issn><eissn>1573-2568</eissn><abstract>Background
Acute pancreatitis is an inflammation of the pancreatic glandular parenchyma that causes injury with or without the destruction of pancreatic acini. Clinical and experimental evidence suggest that certain systemic proinflammatory mediators may be responsible for initiating the fundamental mechanisms involved in microglial reactivity. Here, we investigated the possible repercussions of acute pancreatitis (AP) on the production of inflammatory mediators in the brain parenchyma focusing on microglial activation in the hippocampus.
Methods
The acute pancreatic injury in rats was induced by a pancreas ligation surgical procedure (PLSP) on the splenic lobe, which corresponds to approximately 10% of total mass of the pancreas. Blood samples were collected via intracardiac puncture for the measurement of serum amylase. After euthanasia, frozen or paraffin-embedded brains and pancreas were analyzed using qRT-PCR or immunohistochemistry, respectively.
Results
Immunohistochemistry assays showed a large number of Iba1 and PU.1-positive cells in the CA1, CA3, and dentate gyrus (DG) regions of the hippocampus of the PLSP group. TNF-α mRNA expression was significantly higher in the brain from PLSP group. NLRP3 inflammasome expression was found to be significantly increased in the pancreas and brain of rats of the PLSP group. High levels of BNDF mRNA were found in the rat brain of PLSP group. In contrast, NGF mRNA levels were significantly higher in the control group versus PLSP group.
Conclusion
Our findings suggest that AP has the potential to induce morphological changes in microglia consistent with an activated phenotype.</abstract><cop>New York</cop><pub>Springer US</pub><pmid>37957410</pmid><doi>10.1007/s10620-023-08167-x</doi><tpages>13</tpages><orcidid>https://orcid.org/0000-0001-7847-022X</orcidid></addata></record> |
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subjects | Acute Disease Animals Biochemistry Brain Gastroenterology Hepatology Hippocampus - metabolism Medicine Medicine & Public Health Microglia - metabolism Oncology Original Article Pancreas Pancreas - metabolism Pancreatitis Pancreatitis - metabolism Rats RNA, Messenger - metabolism Transplant Surgery |
title | Hippocampal Microglia Activation Induced by Acute Pancreatic Injury in Rats |
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