Recombinant CCL17-dependent CCR4 activation alleviates neuroinflammation and neuronal apoptosis through the PI3K/AKT/Foxo1 signaling pathway after ICH in mice.
Shuixiang DengPeng JinPrativa SherchanShengpeng LiuYuhui CuiLei HuangJohn H ZhangYe GongJi-Ping TangPublished in: Journal of neuroinflammation (2021)
rCCL17-dependent CCR4 activation ameliorated neurological deficits, reduced brain edema, and ameliorated neuroinflammation and neuronal apoptosis, at least in part, through the PI3K/AKT/Foxo1 signaling pathway after ICH. Thus, activation of CCR4 may provide a promising therapeutic approach for the early management of ICH.
Keyphrases
- signaling pathway
- pi k akt
- cerebral ischemia
- cell cycle arrest
- traumatic brain injury
- dendritic cells
- oxidative stress
- endoplasmic reticulum stress
- regulatory t cells
- epithelial mesenchymal transition
- induced apoptosis
- transcription factor
- lipopolysaccharide induced
- lps induced
- subarachnoid hemorrhage
- brain injury
- white matter
- multiple sclerosis
- type diabetes
- liver injury
- inflammatory response
- liver fibrosis
- functional connectivity
- cell free