Chronic cerebral hypoperfusion (CCH) leads to white matter injury (WMI), a key contributor to the development of vascular cognitive impairment (VCI). Beraprost sodium (BPS) is a chemically stable and orally active prostaglandin I (PGI) analog, while the role and mechanism of BPS in VCI have not been well understood. In this study, we used a mouse model of bilateral carotid artery stenosis (BCAS mice) and demonstrated that BPS treatment facilitated the proliferation and differentiation of oligodendrocyte precursor cells (OPCs), potentially via PDGFR-α pathway modulation.
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