Fasudil alleviates cerebral ischemia‑reperfusion injury by inhibiting inflammation and improving neurotrophic factor expression in rats

The Rho kinase inhibitor fasudil exerts neuroprotective effects. We previously showed that fasudil can regulate M1/M2 microglia polarization and inhibit neuroinflammation. Here, the therapeutic effect of fasudil on cerebral ischemia‑reperfusion (I/R) injury was investigated using the middle cerebral...

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Published inActa neurobiologiae experimentalis Vol. 83; no. 1; p. 97
Main Authors Guo, Min‑Fang, Zhang, Hui‑Yu, Zhang, Pei‑Jun, Zhao, Yi‑Jin, Yu, Jing‑Wen, Meng, Tao, Li, Meng‑Di, Li, Na, Cun‑Ma, Song, Li‑Juan, Yu, Jie‑Zhong
Format Journal Article
LanguageEnglish
Published Warsaw Polish Academy of Sciences 01.01.2023
Subjects
Apoptosis
Brain
Brain injury
Cerebral blood flow
Genotype & phenotype
Head injuries
Inflammation
Inflammatory response
Injury prevention
Ischemia
Kinases
Microglia
Neurological diseases
Neuroprotection
Neurotrophic factors
Occlusion
Phenotypes
Polarization
Reperfusion
Rho-associated kinase
TLR4 protein
Toll-like receptors
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Summary:The Rho kinase inhibitor fasudil exerts neuroprotective effects. We previously showed that fasudil can regulate M1/M2 microglia polarization and inhibit neuroinflammation. Here, the therapeutic effect of fasudil on cerebral ischemia‑reperfusion (I/R) injury was investigated using the middle cerebral artery occlusion and reperfusion (MCAO/R) model in Sprague‑Dawley rats. The effect of fasudil on the phenotype of microglia and neurotrophic factors in the I/R brain and its potential molecular mechanism was also explored. It was found that fasudil ameliorated neurological deficits, neuronal apoptosis, and inflammatory response in rats with cerebral I/R injury. Fasudil also promoted the polarization of microglia into the M2 phenotype, in turn promoting the secretion of neurotrophic factors. Furthermore, fasudil significantly inhibited the expression of TLR4 and NF‑κB. These findings suggest that fasudil could inhibit the neuroinflammatory response and reduce brain injury after I/R injury by regulating the shift of microglia from an inflammatory M1 phenotype to an anti‑inflammatory M2 phenotype, which may be related to the regulation of the TLR4/ NF‑κB signal pathway.
ISSN:0065-1400
1689-0035
DOI:10.55782/ane‑2023‑010