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USP38 protein alleviates neuroinflammation of cerebral ischemia–reperfusion injury via KDM5B expression
Molecular & Cellular Toxicology ( IF 1.7 ) Pub Date : 2021-08-23 , DOI: 10.1007/s13273-021-00154-5
Hongru Wang 1 , Xinhong Xue 1
Affiliation  

Background

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.

Objectives

The experiment investigated that the effects of USP38 in cerebral ischemia–reperfusion injury (CI–RI) and its possible mechanism.

Results

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.

Conclusion

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.



中文翻译:

USP38蛋白通过KDM5B表达减轻脑缺血再灌注损伤的神经炎症

背景

脑血管病是中老年人群常见的慢性病,​​损害严重。及时恢复脑组织中的缺血(即血液再灌注)可以减轻脑损伤。

目标

本实验研究了USP38在脑缺血再灌注损伤(CI-RI)中的作用及其可能机制。

结果

USP38 表达在 CI-RI 模型患者或 CI-RI 模型小鼠中下调。USP38 通过激活 KDM5B 减轻 CI-RI 模型的体外模型或 CI-RI 模型的小鼠模型的神经炎症。在 CI-RI 模型的体外模型中,USP38 蛋白与 KDM5B 蛋白相互关联。KDM5B的调节调节了USP38体外CI-RI模型的作用。

结论

我们的数据表明,USP38 蛋白通过 KDM5B 表达减轻脑缺血再灌注损伤的神经炎症,作为对抗 CI-RI 炎症的新疗法。

更新日期:2021-08-24
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