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Introduction Neonatal hypoxic-ischemic brain damage (HIBD), which is caused by perinatal asphyxia, is a primary etiology for acute neonatal mortality and long-term infant neurological dysfunction ( Endogenous neurogenesis is the process by which neural stem cells (NSCs) undergo symmetric and asymmetric divisions, after which they proliferate and subsequently differentiate into directed progenitor cells that gradually migrate to functional brain areas while undergoing uninterrupted plastic changes and establishing synaptic connections to produce neurological functions (Figure 1)

In macrophages, the activation of mGluR5 elevates the level of the nuclear receptor peroxisome proliferator-activated receptor (PPAR) g and promotes a shift from M1 to M2 phenotype, leading to reduced IFN- production [180]

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