NLRP3 inflammasome-mediated choroid plexus hypersecretion contributes to hydrocephalus after intraventricular hemorrhage via phosphorylated NKCC1 channels.

ABSTRACT:

Background

Hydrocephalus is a severe complication of intracerebral hemorrhage with ventricular extension (ICH-IVH) and causes cerebrospinal fluid (CSF) accumulation. The choroid plexus epithelium plays an important role in CSF secretion and constitutes the blood-CSF barrier within the brain-immune system interface. Although the NLRP3 inflammasome, as a key component of the innate immune system, promotes neuroinflammation, its role in the pathogenesis of hydrocephalus after hemorrhage has not been investigated. Therefore, this study aimed to investigate the potential mechanism of NLRP3 in hydrocephalus to discover a potential marker for targeted therapy.

Methods

A rat model of hydrocephalus after ICH-IVH was developed through autologous blood infusion in wild-type and Nlrp3

SUBMITTER: Zhang Z 

PROVIDER: S-EPMC9210649 | biostudies-literature | 2022 Jun

REPOSITORIES: biostudies-literature