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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
Main Authors: 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
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container_title Digestive diseases and sciences
container_volume 69
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
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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 &amp; 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. 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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. 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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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