CNS neuroscience & therapeutics · 2026
Cystatin B Attenuates Cerebral Ischemia Reperfusion Injury by Inhibiting the JAK2/STAT3 Signaling Pathway.
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Zhou Gang, Hu Fengjiao, Gao Ju, Wang Lei, Wu Xiangbo, Tian Yu, Zhang Peng, Xia Guangming, Wan Feng, Wang Jinhua
Аннотация
BACKGROUND: Cerebral ischemia reperfusion injury (CIRI) poses a significant clinical and economic burden worldwide. Therefore, it is essential to identify key regulators that may improve stroke prognosis. Cystatin B (CSTB) is known to be involved in neuroprotection, inflammation modulation, and apoptosis regulation, but its specific function and mechanisms in CIRI remain unclear.
METHODS: We employed gain- and loss-of-function approaches in a mouse model of transient middle cerebral artery occlusion (t/MCAO) and in cultured neurons subjected to oxygen-glucose deprivation/reperfusion (OGD/R). The effects were evaluated primarily using a combination of quantitative PCR, Western blot, and immunofluorescence staining to assess neurological deficits, inflammatory responses, and apoptosis, as well as to elucidate the underlying mechanisms.
RESULTS: Our findings demonstrated that CSTB significantly attenuated CIRI, as evidenced by the mitigation of neurological deficits, inflammation, and apoptosis. Mechanistically, the protective effects of CSTB were associated with the suppression of the JAK2/STAT3 signaling pathway.
CONCLUSION: This study identifies CSTB as a novel negative regulator of CIRI. Its protective role is mediated through the inhibition of apoptosis and inflammatory responses via the JAK2/STAT3 axis, suggesting its potential as a therapeutic target for ischemic stroke.
METHODS: We employed gain- and loss-of-function approaches in a mouse model of transient middle cerebral artery occlusion (t/MCAO) and in cultured neurons subjected to oxygen-glucose deprivation/reperfusion (OGD/R). The effects were evaluated primarily using a combination of quantitative PCR, Western blot, and immunofluorescence staining to assess neurological deficits, inflammatory responses, and apoptosis, as well as to elucidate the underlying mechanisms.
RESULTS: Our findings demonstrated that CSTB significantly attenuated CIRI, as evidenced by the mitigation of neurological deficits, inflammation, and apoptosis. Mechanistically, the protective effects of CSTB were associated with the suppression of the JAK2/STAT3 signaling pathway.
CONCLUSION: This study identifies CSTB as a novel negative regulator of CIRI. Its protective role is mediated through the inhibition of apoptosis and inflammatory responses via the JAK2/STAT3 axis, suggesting its potential as a therapeutic target for ischemic stroke.