TRPV1 mediates astrocyte activation and interleukin-1β release induced by hypoxic ischemia (HI).

ABSTRACT:

Background

Hypoxic-ischemic encephalopathy (HIE) is a serious birth complication with high incidence in both advanced and developing countries. Children surviving from HIE often have severe long-term sequela including cerebral palsy, epilepsy, and cognitive disabilities. The severity of HIE in infants is tightly associated with increased IL-1β expression and astrocyte activation which was regulated by transient receptor potential vanilloid 1 (TRPV1), a non-selective cation channel in the TRP family.

Methods

Neonatal hypoxic ischemia (HI) and oxygen-glucose deprivation (OGD) were used to simulate HIE in vivo and in vitro. Primarily cultured astrocytes were used for investigating the expression of glial fibrillary acidic protein (GFAP), IL-1β, Janus kinase 2 (JAK2), signal tra

SUBMITTER: Yang XL 

PROVIDER: S-EPMC6540554 | biostudies-literature | 2019 May

REPOSITORIES: biostudies-literature