Edaravone dexborneol alleviates pericyte-mediated fibrosis depositing extracellular matrix through TGF-β1/IL-11 in cerebral small vessel disease.

ABSTRACT:

Background

Chronic cerebral hypoperfusion (CCH) is a critical pathophysiological mechanism underlying cerebral small vessel disease (CSVD). Accumulating evidence have demonstrated that resident pericytes and deposit extracellular matrix (ECM) and play a key role in mediating fibrosis in hypoxic changes. Edaravone dexborneol (EDB) is known to target multiple pathways involved in fibrosis.

Methods

We constructed the CCH mouse models that were subjected to either PBS or EDB at different concentrations. Measures of cognitive function, neuronal damage, white matter lesion (WML), the fibrous profiles of pericytes and ECM protein were investigated to assess the effect of EDB. RNA sequencing of OGD in pericytes was performed to identify a key signaling pathway.

Results

We obs

SUBMITTER: Duan Q 

PROVIDER: S-EPMC11800546 | biostudies-literature | 2025 Feb

REPOSITORIES: biostudies-literature