Cerebrovascular disease is a common chronic disease in the middle-aged and elderly population, with severe damage. Timely restoration of ischemia (ie blood reperfusion) in brain tissue can attenuate brain damage.
The experiment investigated that the effects of USP38 in cerebral ischemia–reperfusion injury (CI–RI) and its possible mechanism.
USP38 expression were down-regulated in patients with CI–RI model or mice with CI–RI model. USP38 alleviates neuroinflammation in vitro model of CI–RI model or mice model of CI–RI model by the activation of KDM5B. USP38 protein was interlinkaged with KDM5B protein in vitro model of CI–RI model. The regulation of KDM5B regulated the effects of USP38 in vitro model of CI–RI model.
Our data demonstrated that USP38 protein alleviates neuroinflammation of cerebral ischemia–reperfusion injury via KDM5B expression, as a novel therapy to counteract inflammation of CI–RI.