Abstract
Aberrant c-Jun N terminal kinase (JNK) activation is broadly involved in the pathogenesis of several acute and chronic neurological diseases. However, the mechanism of JNK activation leading to aggravation of injury after ICH remains unclear. In this study, we confirmed that using NIMoEsh to inhibit JNK activation effectively reduced the level of brain injury following ICH. We evaluated brain outcomes by histology, immunofluorescence, Luxol fast blue/Cresyl violet staining and other experimental methods. We found that NIMoEsh could significantly inhibit the activity of JNK and thus improve inflammation, white-matter damage and neuronal cell death after ICH in mice. Our results suggest that JNK activation plays an important role of brain damage after acute stage of ICH and that NIMoEsh may be a potential target drug for the treatment of ICH.
Published Version
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