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Fig. 2 | Journal of Neuroinflammation

Fig. 2

From: The role of G-CSF neuroprotective effects in neonatal hypoxic-ischemic encephalopathy (HIE): current status

Fig. 2

Schematic illustration of the potential mechanism of G-CSF action in hypoxia ischemia injury. In the acute phase of cerebral ischemia, G-CSF can protect the brain by inhibiting glutamate release, anti-inflammatory, anti-apoptotic, and inhibit edema formation. In subacute phase, GCSFR can stimulate endogenous neuronal regeneration, mobilization of bone marrow stem cells, driving neuronal regeneration and functional repair, and promote neovascularization (angiogenesis and neurogenesis) during the chronic phase

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