Malcok, U. A.Doganlar, O.Tufekcioglu, N. K.Ovali, M. A.Aykora, D.Doganlar, Z. B.Buyuk, B.2024-06-122024-06-1220230091-150X1573-9031https://doi.org/10.1007/s11094-023-02953-7https://hdl.handle.net/20.500.14551/24060Early brain injury (EBI) in the first 24-72 h is the leading cause of mortality and disability related to subarachnoid hemorrhage (SAH). Both melatonin and microRNAs (miRs) are involved in the regulation of a number of neuronal molecular signaling procedures in the central nervous system, ranging from hypoxia, inflammation to neuronal apoptosis. The present study was performed to explore the effect of miRs-17/20 and combined treatment with melatonin on early brain injury after SAH and underlying molecular mechanisms in rats. In this study 54 Wistar albino rats were divided into six experimental groups: Sham, SAH, SAH + Melatonin, SAH+miRs-17/20 control, SAH+MEL+miRs-17/20, and SAH+MEL+miRs-17/20. The Garcia's Neurological Scoring Scale and motor coordination tests were used for clinical observation. H&E staining was performed to evaluate pathological score. The gene expression levels were determined by qRT-PCR and key proteins were quantitated by Western blot assay. miRs-17/20 with or without melatonin treatment suppressed the expression and activity of both the HIF1/VEGF/MMPs and the IL6R/JAK2/STAT3 axis. miRs-17/20 with or without melatonin treatment also mitigated the clinical impairment, pyknosis, and edema in the hippocampus and cortex and neurodegeneration induced by SAH. Our results show that miRs-17/20 alleviated EBI by reducing hypoxic conditions, hypoxia-induced molecular signaling, and neuronal apoptosis.en10.1007/s11094-023-02953-7info:eu-repo/semantics/closedAccessSubarachnoid Hemorrhage Early Brain InjuryMicrornas-17/20MelatoninMitochondrial PathwaySignaling PathwayMir-17-92 ClusterOxidative StressMelatoninActivationApoptosisAutophagyModelHypoxia-Inducible-Factor-1-AlphaArticle576793808N/AWOS:0010848263000072-s2.0-85174254620Q4