BFGF promotes neurological recovery from neonatal hypoxic-ischemic encephalopathy by IL-1β signaling pathway-mediated axon regeneration.

ABSTRACT:

Introduction

Neonatal hypoxia-ischemic brain damage (HIBD) can lead to serious neuron damage and dysfunction, causing a significant worldwide health problem. bFGF as a protective reagent promotes neuron repair under hypoxia/ischemia (HI). However, how bFGF and downstream molecules were regulated in HI remains elusive.

Methods

We established an in vitro HI model by culturing primary cortical neurons and treated with oxygen-glucose deprivation (OGD). We suppressed the expression of bFGF by using siRNA (small interfering RNA) interference to detect the neuronal morphological changes by immunofluorescence staining. To determine the potential mechanisms regulated by bFGF, the change of downstream molecular including IL-1β was examined in bFGF knockdown condition. IL-1β knockout (

SUBMITTER: Ma Z 

PROVIDER: S-EPMC7428497 | biostudies-literature | 2020 Aug

REPOSITORIES: biostudies-literature