BMX deletion mitigates neuroinflammation induced by retinal ischemia/reperfusion through modulation of the AKT/ERK/STAT3 signaling cascade

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DOI: 10.1016/j.heliyon.2024.e27114 Publication Date: 2024-02-24T07:39:24Z
ABSTRACT
AimsRetinal ischemia/reperfusion (I/R) injury is implicated in the etiology of various ocular disorders. Prior research has demonstrated that bone marrow tyrosine kinase on chromosome X (BMX) contributes to advancement ischemic disease and inflammatory reactions. Consequently, current investigation aims evaluate BMX's impact retinal I/R clarify its implied mechanism action.Main methodsThis study utilized male female systemic BMX knockout (BMX−/−) mice conduct experiments. The utilization Western blot assay immunofluorescence labeling techniques was employed investigate variations expression protein tissue localization. Histomorphological changes were observed through H&E staining SD-OCT examination. Visual function assessed electrophysiological Furthermore, apoptosis retina identified using TUNEL assay, as well ELISA technique, which been determine factors level.Key findingsOur results revealed knockdown did not yield a significant effect mouse retina. In mice, mitigated negative structure visual function. effectively reduced apoptosis, suppressed responses, decreased subsequent injury. outcomes partially protected downregulating phosphorylation AKT/ERK/STAT3 pathway.SignificanceOur showed BMX−/− reduces AKT, ERK, STAT3 phosphorylation, reducing inflammation. Thus, this strategy from structural functional damage after
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