Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in Mice

Aim. The protection against ischemia/reperfusion injury mediated by remote limb ischemic postconditioning (RIPC) shows great clinical value in ischemic stroke therapy, but the particular mechanism of RIPC remains unclear. Methods. We carried out middle cerebral artery occlusion/reperfusion (MCAO/R)...

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Main Authors: Dong Han, Jue Wang, Lulu Wen, Miao Sun, Hang Liu, Yan Gao
Format: Article
Language:English
Published: Wiley 2021-01-01
Series:Journal of Immunology Research
Online Access:http://dx.doi.org/10.1155/2021/6688053
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author Dong Han
Jue Wang
Lulu Wen
Miao Sun
Hang Liu
Yan Gao
author_facet Dong Han
Jue Wang
Lulu Wen
Miao Sun
Hang Liu
Yan Gao
author_sort Dong Han
collection DOAJ
description Aim. The protection against ischemia/reperfusion injury mediated by remote limb ischemic postconditioning (RIPC) shows great clinical value in ischemic stroke therapy, but the particular mechanism of RIPC remains unclear. Methods. We carried out middle cerebral artery occlusion/reperfusion (MCAO/R) surgery on C57BL/6 male mice. RIPC was generated by 10-minute occlusion followed by the same period of reperfusion of the bilateral hind limb femoral artery and repeated for 3 cycles. Infarct size and neurological score were performed to assess stroke outcomes. Ly6Chi monocytes were quantified in the blood and brain by flow cytometry. Real-time PCR, ELISA, and immunofluorescence were utilized to detect phenotype of proinflammatory M1 and anti-inflammatory M2 microglia/macrophage. Nuclear factor κB (NF-κB) and peroxisome proliferator-activated receptor γ (PPARγ) levels were detected using Western blot. Results. At 24 and 72 h after MCAO, RIPC drastically attenuated infarct size and ameliorated the neurological deficits of mice and facilitated transmigration of Ly6Chi monocytes to the brain postischemia reperfusion. Furthermore, RIPC contributed to increased M2 and reduced M1 microglia/macrophage through inhibiting NF-κB and promoting PPARγ activation. Conclusion. Our results reveal pharmacological effect of RIPC in promoting microglia/macrophage transferring from M1 to M2 phenotype after MCAO/R in mice, which provides theoretical support for the therapeutic effect of RIPC in ischemic stroke.
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institution Kabale University
issn 2314-8861
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publishDate 2021-01-01
publisher Wiley
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spelling doaj-art-6d643c7ea92741089081a595356e05492025-02-03T01:20:48ZengWileyJournal of Immunology Research2314-88612314-71562021-01-01202110.1155/2021/66880536688053Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in MiceDong Han0Jue Wang1Lulu Wen2Miao Sun3Hang Liu4Yan Gao5Department of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, Shenyang 110004, ChinaDepartment of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, Shenyang 110004, ChinaDepartment of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, Shenyang 110004, ChinaDepartment of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, Shenyang 110004, ChinaDepartment of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, Shenyang 110004, ChinaDepartment of Neurology, Shengjing Hospital of China Medical University, 36 Sanhao Street, Heping District, Shenyang 110004, ChinaAim. The protection against ischemia/reperfusion injury mediated by remote limb ischemic postconditioning (RIPC) shows great clinical value in ischemic stroke therapy, but the particular mechanism of RIPC remains unclear. Methods. We carried out middle cerebral artery occlusion/reperfusion (MCAO/R) surgery on C57BL/6 male mice. RIPC was generated by 10-minute occlusion followed by the same period of reperfusion of the bilateral hind limb femoral artery and repeated for 3 cycles. Infarct size and neurological score were performed to assess stroke outcomes. Ly6Chi monocytes were quantified in the blood and brain by flow cytometry. Real-time PCR, ELISA, and immunofluorescence were utilized to detect phenotype of proinflammatory M1 and anti-inflammatory M2 microglia/macrophage. Nuclear factor κB (NF-κB) and peroxisome proliferator-activated receptor γ (PPARγ) levels were detected using Western blot. Results. At 24 and 72 h after MCAO, RIPC drastically attenuated infarct size and ameliorated the neurological deficits of mice and facilitated transmigration of Ly6Chi monocytes to the brain postischemia reperfusion. Furthermore, RIPC contributed to increased M2 and reduced M1 microglia/macrophage through inhibiting NF-κB and promoting PPARγ activation. Conclusion. Our results reveal pharmacological effect of RIPC in promoting microglia/macrophage transferring from M1 to M2 phenotype after MCAO/R in mice, which provides theoretical support for the therapeutic effect of RIPC in ischemic stroke.http://dx.doi.org/10.1155/2021/6688053
spellingShingle Dong Han
Jue Wang
Lulu Wen
Miao Sun
Hang Liu
Yan Gao
Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in Mice
Journal of Immunology Research
title Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in Mice
title_full Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in Mice
title_fullStr Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in Mice
title_full_unstemmed Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in Mice
title_short Remote Limb Ischemic Postconditioning Protects against Ischemic Stroke via Modulating Microglia/Macrophage Polarization in Mice
title_sort remote limb ischemic postconditioning protects against ischemic stroke via modulating microglia macrophage polarization in mice
url http://dx.doi.org/10.1155/2021/6688053
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