Artesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia

Objective Inflammation is an important factor in the pathological process of cerebral ischemia. Artesunate exhibits a broad range of anti-inflammatory properties in many diseases. We investigated the potential protective effect of artesunate against cerebral ischemia and the related mechanisms. Meth...

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Autores principales: Ying Liu, Wei Dang, Shiyang Zhang, Lina Wang, Xiangjian Zhang
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Lenguaje:EN
Publicado: SAGE Publishing 2021
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Acceso en línea:https://doaj.org/article/594ac9c249594cfca40dab3d736ae853
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spelling oai:doaj.org-article:594ac9c249594cfca40dab3d736ae8532021-11-09T01:03:21ZArtesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia1473-230010.1177/03000605211053549https://doaj.org/article/594ac9c249594cfca40dab3d736ae8532021-11-01T00:00:00Zhttps://doi.org/10.1177/03000605211053549https://doaj.org/toc/1473-2300Objective Inflammation is an important factor in the pathological process of cerebral ischemia. Artesunate exhibits a broad range of anti-inflammatory properties in many diseases. We investigated the potential protective effect of artesunate against cerebral ischemia and the related mechanisms. Methods Mice were divided into distal middle cerebral artery occlusion (dMCAO), sham, low dose, and high dose groups and subjected to dMCAO, except for the sham group. The low and high dose groups were administered artesunate (15 and 30 mg/kg), and the neuroprotective effects were analyzed by evaluating infarct volumes and neurological deficits. Microglial activation and neutrophil infiltration were evaluated by immunofluorescence, immunohistochemical staining, and western blotting. Inflammatory mediators were measured by enzyme-linked immunosorbent assays. Nuclear factor (NF)-κB nuclear translocation was detected by immunofluorescence and western blotting. Results Compared with the dMCAO group, artesunate significantly improved neurological deficit scores and infarct volumes and ameliorated inflammation by reducing neutrophil infiltration, suppressing microglial activation, and downregulating tumor necrosis factor-α and interleukin-1β expression. Furthermore, artesunate inhibited nuclear translocation of NF-κB and inhibitor protein α proteolysis. Conclusions Artesunate protected against inflammatory injury by reducing neutrophil infiltration and microglial activation, suppressing inflammatory cytokines, and inhibiting the NF-κB pathway. Therefore, artesunate is a potential ischemic stroke treatment.Ying LiuWei DangShiyang ZhangLina WangXiangjian ZhangSAGE PublishingarticleMedicine (General)R5-920ENJournal of International Medical Research, Vol 49 (2021)
institution DOAJ
collection DOAJ
language EN
topic Medicine (General)
R5-920
spellingShingle Medicine (General)
R5-920
Ying Liu
Wei Dang
Shiyang Zhang
Lina Wang
Xiangjian Zhang
Artesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia
description Objective Inflammation is an important factor in the pathological process of cerebral ischemia. Artesunate exhibits a broad range of anti-inflammatory properties in many diseases. We investigated the potential protective effect of artesunate against cerebral ischemia and the related mechanisms. Methods Mice were divided into distal middle cerebral artery occlusion (dMCAO), sham, low dose, and high dose groups and subjected to dMCAO, except for the sham group. The low and high dose groups were administered artesunate (15 and 30 mg/kg), and the neuroprotective effects were analyzed by evaluating infarct volumes and neurological deficits. Microglial activation and neutrophil infiltration were evaluated by immunofluorescence, immunohistochemical staining, and western blotting. Inflammatory mediators were measured by enzyme-linked immunosorbent assays. Nuclear factor (NF)-κB nuclear translocation was detected by immunofluorescence and western blotting. Results Compared with the dMCAO group, artesunate significantly improved neurological deficit scores and infarct volumes and ameliorated inflammation by reducing neutrophil infiltration, suppressing microglial activation, and downregulating tumor necrosis factor-α and interleukin-1β expression. Furthermore, artesunate inhibited nuclear translocation of NF-κB and inhibitor protein α proteolysis. Conclusions Artesunate protected against inflammatory injury by reducing neutrophil infiltration and microglial activation, suppressing inflammatory cytokines, and inhibiting the NF-κB pathway. Therefore, artesunate is a potential ischemic stroke treatment.
format article
author Ying Liu
Wei Dang
Shiyang Zhang
Lina Wang
Xiangjian Zhang
author_facet Ying Liu
Wei Dang
Shiyang Zhang
Lina Wang
Xiangjian Zhang
author_sort Ying Liu
title Artesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia
title_short Artesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia
title_full Artesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia
title_fullStr Artesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia
title_full_unstemmed Artesunate attenuates inflammatory injury and inhibits the NF-κB pathway in a mouse model of cerebral ischemia
title_sort artesunate attenuates inflammatory injury and inhibits the nf-κb pathway in a mouse model of cerebral ischemia
publisher SAGE Publishing
publishDate 2021
url https://doaj.org/article/594ac9c249594cfca40dab3d736ae853
work_keys_str_mv AT yingliu artesunateattenuatesinflammatoryinjuryandinhibitsthenfkbpathwayinamousemodelofcerebralischemia
AT weidang artesunateattenuatesinflammatoryinjuryandinhibitsthenfkbpathwayinamousemodelofcerebralischemia
AT shiyangzhang artesunateattenuatesinflammatoryinjuryandinhibitsthenfkbpathwayinamousemodelofcerebralischemia
AT linawang artesunateattenuatesinflammatoryinjuryandinhibitsthenfkbpathwayinamousemodelofcerebralischemia
AT xiangjianzhang artesunateattenuatesinflammatoryinjuryandinhibitsthenfkbpathwayinamousemodelofcerebralischemia
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