Inhibition of miR-34a ameliorates cerebral ischemia/reperfusion injury by targeting brain-derived neurotrophic factor
Archives of Medical Science(2021)
摘要
IntroductionOxidative stress and neuronal apoptosis are strongly associated with the pathogenesis of ischemic stroke. In this study, we aimed to determine whether miR-34a was involved in ischemia/reperfusion (I/R) injury, oxidative stress, and neuronal apoptosis by targeting brain-derived neurotrophic factor (BDNF).Material and methodsRats received middle cerebral artery occlusion (MCAO) surgery to simulate I/R injury. At 24 h after MCAO surgery, neurological deficits and infarct volumes were evaluated according to Longa’s scale and 2,3,5-triphenyltetrazolium (TTC) chloride staining. Neuronal apoptosis was assessed by terminal deoxynucleotidyl transferase-mediated dUTP nick-end labeling (TUNEL), and the expression of miR-34a and associated proteins were detected by quantitative reverse-transcription polymerase chain reaction (qRT-PCR), and western blotting. Several markers of oxidative stress were detected using commercial kits, and the interaction between miR-34a and BDNF was measured by RNA immunoprecipitation (RIP).ResultsThe results showed that miR-34a was upregulated (p < 0.05), whereas BDNF was downregulated (p < 0.05) in the MCAO rats, and this negative correlation was accompanied by clear oxidative stress and neuronal apoptosis. RIP demonstrated a clear interaction between miR-34a and BDNF. Furthermore, miR-34a was also found to inhibit oxidative stress and neuronal apoptosis, increase BDNF expression, and ameliorate neurological deficits and infarct volumes (p < 0.05) seen in the MCAO rats.ConclusionsThese data suggested that inhibition of miR-34a ameliorated cerebral ischemia/reperfusion injury by targeting BDNF. This mechanism represents a novel and promising target for the treatment of strokes.
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