Edaravone dexborneol Alleviates Pericyte-Mediated Fibrosis Depositing Extracellular matrix through Cerebral Small Vessel Disease

Background: Chronic cerebral hypoperfusion (CCH) is a vital pathophysiological mechanism of cerebral small vessel disease (CSVD). Accumulating evidence proved that resident pericytes originated from the neurovascular unit and deposit extracellular matrix (ECM) mediating fibrosis in hypoxic changes. Edaravone dexborneol (EDB) has multiple targets in neurological impairment, inflammation and fibrosis across a range of disease conditions including stroke, but its effects against CCH pathologies remain to be elucidated.Methods: We constructed the CCH mouse models that were subjected to either PBS or EDB with different concentration. Measures of cognitive function, neuronal damage, white matter lesion (WML), the fibrous profiles of pericytes and ECM protein were investigated the effect of EDB. RNA sequencing of OGD in pericytes was performed to screen a key signaling pathway.