ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK Pathway
Postoperative cognitive dysfunction (POCD) is a well-known complication after surgery with cognitive impairments. Angiopoietin-like protein 2 (ANGPTL2) has been found to be associated with inflammation. However, the role of ANGPTL2 in inflammation of POCD is unclear. Here, mice were subjected into i...
Main Authors: | , , , , , |
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Format: | Article |
Language: | English |
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Hindawi Limited
2023-01-01
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Series: | Mediators of Inflammation |
Online Access: | http://dx.doi.org/10.1155/2023/2453402 |
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author | Xiaoyan Huang Zegeng Su Shuncai Zhang Xiaoling Xu Bo Yang Xiang Xu |
author_facet | Xiaoyan Huang Zegeng Su Shuncai Zhang Xiaoling Xu Bo Yang Xiang Xu |
author_sort | Xiaoyan Huang |
collection | DOAJ |
description | Postoperative cognitive dysfunction (POCD) is a well-known complication after surgery with cognitive impairments. Angiopoietin-like protein 2 (ANGPTL2) has been found to be associated with inflammation. However, the role of ANGPTL2 in inflammation of POCD is unclear. Here, mice were subjected into isoflurane anesthesia. It was demonstrated that isoflurane increased ANGPTL2 expression and promoted pathological change in brain tissues. However, downregulation of ANGPTL2 alleviated the pathological change and elevated learning and memory abilities, improving isoflurane-induced cognitive dysfunction in mice. In addition, isoflurane-induced cell apoptosis and inflammation were repressed via ANGPTL2 knockdown in mice. Downregulation of ANGPTL2 was also verified to suppress isoflurane-induced microglial activation, evidenced by a decrease of Iba1 and CD86 expressions and an increase of CD206 expression. Further, the isoflurane-induced MAPK signaling pathway was repressed through downregulation of ANGPTL2 in mice. In conclusion, this study proved that downregulation of ANGPTL2 attenuated isoflurane-induced neuroinflammation and cognitive dysfunction in mice via modulating the MAPK pathway, which provided a new therapeutic target for POCD. |
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id | doaj.art-951b7b740c484f4bb7c08624976b5682 |
institution | Directory Open Access Journal |
issn | 1466-1861 |
language | English |
last_indexed | 2024-04-10T00:21:10Z |
publishDate | 2023-01-01 |
publisher | Hindawi Limited |
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series | Mediators of Inflammation |
spelling | doaj.art-951b7b740c484f4bb7c08624976b56822023-03-16T00:00:13ZengHindawi LimitedMediators of Inflammation1466-18612023-01-01202310.1155/2023/2453402ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK PathwayXiaoyan Huang0Zegeng Su1Shuncai Zhang2Xiaoling Xu3Bo Yang4Xiang Xu5Department of AnesthesiologyDepartment of AnesthesiologyDepartment of AnesthesiologyDepartment of AnesthesiologyDepartment of AnesthesiologyDepartment of AnesthesiologyPostoperative cognitive dysfunction (POCD) is a well-known complication after surgery with cognitive impairments. Angiopoietin-like protein 2 (ANGPTL2) has been found to be associated with inflammation. However, the role of ANGPTL2 in inflammation of POCD is unclear. Here, mice were subjected into isoflurane anesthesia. It was demonstrated that isoflurane increased ANGPTL2 expression and promoted pathological change in brain tissues. However, downregulation of ANGPTL2 alleviated the pathological change and elevated learning and memory abilities, improving isoflurane-induced cognitive dysfunction in mice. In addition, isoflurane-induced cell apoptosis and inflammation were repressed via ANGPTL2 knockdown in mice. Downregulation of ANGPTL2 was also verified to suppress isoflurane-induced microglial activation, evidenced by a decrease of Iba1 and CD86 expressions and an increase of CD206 expression. Further, the isoflurane-induced MAPK signaling pathway was repressed through downregulation of ANGPTL2 in mice. In conclusion, this study proved that downregulation of ANGPTL2 attenuated isoflurane-induced neuroinflammation and cognitive dysfunction in mice via modulating the MAPK pathway, which provided a new therapeutic target for POCD.http://dx.doi.org/10.1155/2023/2453402 |
spellingShingle | Xiaoyan Huang Zegeng Su Shuncai Zhang Xiaoling Xu Bo Yang Xiang Xu ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK Pathway Mediators of Inflammation |
title | ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK Pathway |
title_full | ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK Pathway |
title_fullStr | ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK Pathway |
title_full_unstemmed | ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK Pathway |
title_short | ANGPTL2 Deletion Attenuates Neuroinflammation and Cognitive Dysfunction Induced by Isoflurane in Aged Mice through Modulating MAPK Pathway |
title_sort | angptl2 deletion attenuates neuroinflammation and cognitive dysfunction induced by isoflurane in aged mice through modulating mapk pathway |
url | http://dx.doi.org/10.1155/2023/2453402 |
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