Activation of MC1R with BMS-470539 attenuates neuroinflammation via cAMP/PKA/Nurr1 pathway after neonatal hypoxic-ischemic brain injury in rats.

Shufeng YuDesislava Met DoychevaMarcin GamdzykYijun YangCameron LenahanGaigai LiDujuan LiLifei LianJiping TangJun LuArne P Neyrinck

Published in: Journal of neuroinflammation (2021)

Our study demonstrated that activation of MC1R with BMS-470539 attenuated neuroinflammation, and improved neurological deficits after neonatal hypoxic-ischemic brain injury in rats. Such anti-inflammatory and neuroprotective effects were mediated, at least in part, via the cAMP/PKA/Nurr1 signaling pathway. Therefore, MC1R activation might be a promising therapeutic target for infants with hypoxic-ischemic encephalopathy (HIE).

Keyphrases

cerebral ischemia
traumatic brain injury
signaling pathway
anti inflammatory
white matter
resting state
cognitive impairment
binding protein
lps induced
early onset
epithelial mesenchymal transition
functional connectivity
subarachnoid hemorrhage
oxidative stress
multiple sclerosis