Vascular cognitive impairment (VCI) is a syndrome defined as cognitive decline caused by vascular disease, which is associated with Alzheimer's disease and vascular dementia. Since chronic cerebral hypoperfusion (CCH) is commonly present in various types of dementia and induces VCI, we used bilateral common carotid artery stenosis (BCAS) mice as a CCH-induced VCI model.　Transient receptor potential ankyrin 1 (TRPA1), the most redox-sensitive TRP channel, is functionally expressed in the brain and seems to function as a polymodal sensor in vascular disease. To clarify the involvement of TRPA1 in CCH-induced VCI, we used genetically engineered mice: TRPA1-knockout (TRPA1-KO) and cell-specific conditional TRPA1-KO mice. We showed that TRPA1 deficiency exacerbated BCAS-induced cognitive impairment and white matter injury during early-stage CCH. TRPA1 stimulation with cinnamaldehyde ameliorated BCAS-induced outcomes. We also revealed that BCAS increased a cytokine in astrocytes. Moreover, TRPA1-stimulated primary astrocyte cultures expressed the cytokine, and culture medium derived from these TRPA1-stimulated cells promoted oligodendrocyte precursor cell myelination. Overall, TRPA1 stimulation in astrocytes plays a protective role in CCH-induced VCI through the cytokine production.