biostudies-literatureXiong JGeneral Program of National Natural Science Foundation of ChinaLiaoning Provincial Science and Technology ProgramScience and Technology Innovation Fund of Daliane0332698https://www.ebi.ac.uk/biostudies/studies/S-EPMC12445528biostudies-literatureUnknown20(9)Cerebral ischemia-reperfusion injury (CIRI) occurs during the treatment of ischemic stroke when the affected blood vessels are recanalized and the oxygen supply to the brain is restored. Chloride intracellular channel 1 (CLIC1) and the nuclear factor erythroid-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway have been implicated in many neurological disorders. However, the exact mechanism by which CLIC1 contributes to CIRI remains unclear, and its potential role in modulating the Nrf2/HO-1 signaling pathway in CIRI has yet to be explored. We investigated the potential roles of CLIC1 in CIRI using an oxygen and glucose deprivation/reoxygenation (OGD/R) model in HT22 cells. The findings of our study indicated that CLIC1 was high-expressed after OGD/R and had an inhibitory effect on thPloS oneCLIC1 down-regulates Nrf2/HO-1 signalling pathway promoting the apoptosis and pyroptosis in OGD/R-treated HT22 cells.PMC124455282021JJ12SN38820719112022-MS-329Xiong JWu JLi SYu CCao YSun CQu XChen HZhang AfalseCLIC1 down-regulates Nrf2/HO-1 signalling pathway promoting the apoptosis and pyroptosis in OGD/R-treated HT22 cells.Cerebral ischemia-reperfusion injury (CIRI) occurs during the treatment of ischemic stroke when the affected blood vessels are recanalized and the oxygen supply to the brain is restored. Chloride intracellular channel 1 (CLIC1) and the nuclear factor erythroid-related factor 2 (Nrf2)/heme oxygenase-1 (HO-1) pathway have been implicated in many neurological disorders. However, the exact mechanism by which CLIC1 contributes to CIRI remains unclear, and its potential role in modulating the Nrf2/HO-1 signaling pathway in CIRI has yet to be explored. We investigated the potential roles of CLIC1 in CIRI using an oxygen and glucose deprivation/reoxygenation (OGD/R) model in HT22 cells. The findings of our study indicated that CLIC1 was high-expressed after OGD/R and had an inhibitory effect on th2025-01-01T00:00:00Z20252026-06-03T14:58:21.435Z2026-04-28T03:11:42.585ZS-EPMC124455284096623810.1371/journal.pone.0332698