Inhibition of miR-19a protects neurons against ischemic stroke through modulating glucose metabolism and neuronal apoptosis.

摘要: Accumulating evidence has shown that altered microRNA (miR) modulation is implicated in the pathologies of ischemic stroke. However, it unclear whether and how hsa-miR-19a-3p mediates cerebral injury. Herein, we investigated functional role miR-19a-3p injury explored its underlying regulatory mechanism. In vivo ischemic/reperfusion (I/R) neuronal vitro oxygen-glucose deprivation (OGD) were established. Expression was determined by quantitative real-time polymerase chain reaction (qRT-PCR). Glucose uptake, lactate production, apoptosis determined. ADIPOR2 predicted as a target silico experimentally validated qRT-PCR, Western blot analysis luciferase assay assays. MiR-19a expression significantly downregulated upregulated rat neurons astrocytes, respectively (P < 0.01). A elevated level found I/R OGD models comparison to sham/control groups glycolysis enzyme markers LDHA, PKM2, HK2, Glut1 PDK1, apoptosis-related factors levels, apoptosis, glucose production repressed both (P < 0.01 each case). Moreover, mimic aggravated, while inhibitor alleviated, above observations. Adipor2 confirmed be direct miR-19a. Furthermore, restoration reversed miR-19a-3p-induced effects. Collectively, our results indicate targeting ADIPOR2. MiR-19a-3p attenuation thus might offer hope novel therapeutic for stroke treatment.