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MicroRNA-32-3p facilitates cerebral ischemia/reperfusion injury through inhibiting Cab39/AMPK 1 1 Introduction 1 2 Materials and methods 2 2.1 Materials 2 2.2 Cell isolation and treatment 2 2.3 Cell viability and LDH releases 2 2.4 Western blot and quantitative real-time PCR 2 2.5 Caspase-3 activity 2 2.6 TUNEL staining 3 2.7 Detection of oxidative stress 3 2.8 Fluorescence in situ hybridization (FISH) assay 3 2.9 Animal studies 3 2.10 Infarct size measurement 3 2.11 Evaluation of neurological deficit 3 2.12 Brain edema analysis 3 2.13 Luciferase reporter assay 3 2.14 Statistical analysis 3 3 Results 3 3.1 The miR-32-3p antagomir prevents OGD/R-induced neural death and oxidative damage in vitro 3 3.2 The miR-32-3p agomir exacerbates OGD/R-induced neural death and oxidative damage in vitro 4 3.3 The miR-32-3p antagomir prevents I/R-induced neural death and oxidative damage in vivo 4 3.4 The miR-32-3p agomir exacerbates I/R-induced neural death and oxidative damage in vivo 6 3.5 The miR-32-3p antagomir improves cerebral I/R injury through activating AMPK 6 3.6 The miR-32-3p antagomir activates AMPK through upregulating Cab39 6 4 Discussion 7 Funding 8 CRediT authorship contribution s

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Language

UND

Category

nonfiction