Inhibition of CCR2 attenuates neuroinflammation and neuronal apoptosis after subarachnoid hemorrhage through the PI3K/Akt pathway.
Qi TianYujia GuoShi FengChengli LiuPeibang HeJianfeng WangWenrui HanChen YangZhan ZhangMingchang LiPublished in: Journal of neuroinflammation (2022)
CCR2 expression was upregulated in both in vitro and in vivo SAH models. Additionally, inhibition of CCR2, at least partly through the PI3K/AKT pathway, alleviated neuroinflammation and neuronal apoptosis in vivo and in vitro. CCR2 levels in the CSF have a moderate diagnostic value for 6-month outcome prediction in patients with SAH.
Keyphrases
- cerebral ischemia
- subarachnoid hemorrhage
- dendritic cells
- regulatory t cells
- brain injury
- oxidative stress
- endoplasmic reticulum stress
- blood brain barrier
- cell cycle arrest
- cell death
- traumatic brain injury
- lipopolysaccharide induced
- poor prognosis
- lps induced
- cognitive impairment
- high intensity
- inflammatory response
- immune response
- long non coding rna