Abstract
As a common complication of diabetes, diabetic pain neuropathy (DPN) is caused by neuron intrinsic and extrinsic factors. Neuron intrinsic factors include neuronal apoptosis and oxidative stress, while extrinsic factors are associated with glial activation. The present study was performed to reveal the functions of miR-130a-3p in apoptosis and oxidative stress of the high glucose (HG)-stimulated primary neurons as well as in the activation of microglial and astrocytes. Primary neurons, microglial, and astrocytes were isolated from newborn mice. Apoptosis was assessed by flow cytometry analysis and western blotting. Reactive oxygen species and glutathione levels were assessed to determine the oxidative stress. Markers of glial cells were detected by immunofluorescence staining. The results revealed that miR-130a-3p deficiency alleviated apoptosis and oxidative stress of HG-stimulated neurons as well as suppressed microglial and astrocyte activation. Moreover, sphingosine-1-phosphate receptor 1 (S1PR1) was found as a target downstream of miR-130a-3p. S1PR1 knockdown partially rescued the inhibitory effects of silenced miR-130a-3p on neuronal injury and glial activation. In conclusion, miR-130a-3p targets S1PR1 to activate the microglial and astrocytes and to promote apoptosis and oxidative stress of the HG-stimulated primary neurons. These findings may provide a novel insight into DPN treatment.