ag-490 and Brain-Injuries--Traumatic

Traumatic brain injury (TBI) is induced by complex primary and secondary mechanisms that give rise to cell death, inflammation, and neurological dysfunction. Understanding the mechanisms that drive neurological damage as well as those that promote repair can guide the development of therapeutic drugs for TBI. Kruppel-like factor 4 (KLF4) has been reported to negatively regulate axon regeneration of injured retinal ganglion cells (RGCs) through inhibition of JAK-STAT3 signaling. However, the role of KLF4 in TBI remains unreported. Reactive oxygen species (ROS)-induced neuronal death is a pathophysiological hallmark of TBI.. In this study, we used H. The results show that H. These findings provide evidence that KLF4 plays an important role in the pathophysiology of TBI. Blocking KLF4 may be a potential therapeutic strategy for the treatment of TBI, either alone or in combination with agents that target complementary mechanisms.

Topics: Animals; Apoptosis; Brain Injuries, Traumatic; Cerebral Cortex; Cyclin D1; Disease Models, Animal; Enzyme Inhibitors; Gene Expression Regulation; Hydrogen Peroxide; Janus Kinases; Kruppel-Like Factor 4; Kruppel-Like Transcription Factors; Nerve Regeneration; Optic Nerve Injuries; Rats; Rats, Sprague-Dawley; Retinal Ganglion Cells; Signal Transduction; STAT3 Transcription Factor; Tumor Suppressor Protein p53; Tyrphostins