Artesunate attenuates inflammation and neurological impairment in intracerebral hemorrhage mice by inhibiting microglia NLRP3/ASC/Caspase-1
- 1Department of Neurosurgery, Xi'an Central Hospital, Xi'an Jiaotong University, Xi'an, China
Abstract
Intracerebral hemorrhage (ICH) impairs brain function through several mechanisms, including local inflammation, which exacerbates neuronal injury. Given the complex pathology of ICH, understanding how to mitigate these effects is essential for improving recovery outcomes. While artesunate (ART) has been recognized for its neuroprotective effects, its role in neural recovery following ICH remains unclear. This study aimed to address this gap by investigating the potential neuroprotective role of ART in ICH recovery. We employed a male C57BL/6 mouse model of ICH and administered ART post-injury. Brain samples were collected three days later for analysis. Hematoxylin and eosin staining was used to assess localized damage, and brain edema was measured using the dry/wet weight method. Neurological function was evaluated through the modified neurological severity score (mNSS) and the corner test. Local inflammation was assessed by measuring interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and myeloperoxidase (MPO). NLRP3/ASC/Caspase-1 expression was analyzed via western blotting to evaluate pyroptosis. Immunofluorescence analysis revealed that microglia predominantly undergo pyroptosis. In vitro, ART inhibited NLRP3-mediated pyroptosis in microglia and reduced the secretion of IL-1β and IL-18. Ultimately, ART decreased neuronal apoptosis, promoted neurogenesis, and improved neurological function after ICH. Our findings suggest that ART may alleviate ICH damage by downregulating NLRP3-mediated microglial pyroptosis, reducing neuronal apoptosis, and decreasing inflammation, offering promising potential for improved ICH treatment and prevention.
Related
- Quercetin attenuates acute inflammation and extracellular matrix remodeling after intracerebral hemorrhage: transcriptomics-informed network pharmacology and experimental validation
- PINK1 agonist MTK458 attenuates cerebral edema by protecting blood-brain barrier integrity in intracerebral hemorrhage mice
- TRPC3 Mediates Neurological Dysfunction after Intracerebral Hemorrhage in Mice
- Ixodes ricinus‐Contact Phase Inhibitor Promotes Functional Recovery and Attenuates Neutrophil Associated Neuroinflammation After Experimental Intracerebral Hemorrhage
- Targeting Ninjurin-1-Mediated Microglial Pyroptosis Attenuates Neuroinflammation and Neuronal Injury Following Intracerebral Hemorrhage.
BibTeX
@article{luo2026artesunate,
title = {{Artesunate attenuates inflammation and neurological impairment in intracerebral hemorrhage mice by inhibiting microglia NLRP3/ASC/Caspase-1}},
author = {Qiang Luo and Yuan Chai and Geng Qin and Yiwen Ma and Zhixiong Zhou and Xiaohuan Huang and Junxiu Xi and Yu Miao},
journal = {Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas},
year = {2026},
month = oct,
doi = {10.1590/1414-431x2026e14465},
url = {https://europepmc.org/article/PMC/PMC13722007},
note = {CC BY},
}
RIS
TY - JOUR
TI - Artesunate attenuates inflammation and neurological impairment in intracerebral hemorrhage mice by inhibiting microglia NLRP3/ASC/Caspase-1
AU - Qiang Luo
AU - Yuan Chai
AU - Geng Qin
AU - Yiwen Ma
AU - Zhixiong Zhou
AU - Xiaohuan Huang
AU - Junxiu Xi
AU - Yu Miao
PY - 2026
DA - 2026/10/01
JO - Brazilian journal of medical and biological research = Revista brasileira de pesquisas medicas e biologicas
DO - 10.1590/1414-431x2026e14465
UR - https://europepmc.org/article/PMC/PMC13722007
AB - Intracerebral hemorrhage (ICH) impairs brain function through several mechanisms, including local inflammation, which exacerbates neuronal injury. Given the complex pathology of ICH, understanding how to mitigate these effects is essential for improving recovery outcomes. While artesunate (ART) has been recognized for its neuroprotective effects, its role in neural recovery following ICH remains unclear. This study aimed to address this gap by investigating the potential neuroprotective role of ART in ICH recovery. We employed a male C57BL/6 mouse model of ICH and administered ART post-injury. Brain samples were collected three days later for analysis. Hematoxylin and eosin staining was used to assess localized damage, and brain edema was measured using the dry/wet weight method. Neurological function was evaluated through the modified neurological severity score (mNSS) and the corner test. Local inflammation was assessed by measuring interleukin (IL)-1β, tumor necrosis factor (TNF)-α, and myeloperoxidase (MPO). NLRP3/ASC/Caspase-1 expression was analyzed via western blotting to evaluate pyroptosis. Immunofluorescence analysis revealed that microglia predominantly undergo pyroptosis. In vitro, ART inhibited NLRP3-mediated pyroptosis in microglia and reduced the secretion of IL-1β and IL-18. Ultimately, ART decreased neuronal apoptosis, promoted neurogenesis, and improved neurological function after ICH. Our findings suggest that ART may alleviate ICH damage by downregulating NLRP3-mediated microglial pyroptosis, reducing neuronal apoptosis, and decreasing inflammation, offering promising potential for improved ICH treatment and prevention.
SN - 0100-879X
SN - 1414-431X
ER -