G protein and MYD Growth Factor in neuroprotection after cerebral ischemia-reperfusion

To explore the neuroprotective role of Myeloid-Derived Growth Factor (MYDGF) and its regulatory mechanisms involving G protein-coupled signaling pathways after cerebral ischemia-reperfusion injury (CIRI). A mouse model of CIRI was established using middle cerebral artery occlusion (MCAO). Mice were divided into five groups: Mock, scramble shRNA (sh-scr), MYDGF knockdown (MYDGF-shRNA), Gαi1/3 knockdown (Gαi1/3-shRNA), and recombinant MYDGF treatment. MYDGF mRNA expression was analyzed using qRT-PCR, and protein levels were assessed via Western blot. Cell-type specific knockdown in glial cells was achieved using targeted adenoviral shRNA. MYDGF exerted neuroprotective effects by activating PI3K-AKT-mTOR and ERK-MAPK signaling pathways. Gαi1/3 was identified as a key regulatory factor mediating these effects. MYDGF exerted neuroprotective effects by activating PI3K-AKT-mTOR and ERK-MAPK signaling pathways. Gαi1/3 was identified as a key regulatory factor mediating these effects.