MiR-325-5p Targets HDAC3 to Protect Early Brain Injury in Subarachnoid Hemorrhage via NF-κB Signal Pathway

Abstract

Objective: To explore miR-325-5p expression after subarachnoid hemorrhage (SAH) and its impact on early brain injury in SAH rats. Methods: Forty-eight male Sprague-Dawley (SD) rats were used in this study, 12 in the sham group, 12 in the SAH group, 12 in the SAH+miR-325-5p mimic group, and 12 in SAH+miR-325-5p mimic+oe-HDAC3 group. The SAH model was established using a common occipital cistern secondary blood injection. Brain water content and SAH grades were measured. Quantitative real time reverse transcription polymerase chain reaction (qRT-PCR) assay was used to measure miR-325-5p expression. Apoptosis was assessed by flow cytometry. Cell Counting Kit-8 (CCK8) assay was used to examine cell proliferation. Luciferase reporter assay was used to confirm the relationship between miR-325-5p and HDAC3 (histone deacetylase 3). Results: MiR-325-5p expression decreased in the SAH rats and oxyHb induced PC12 cells. Apoptosis decreased induced by miR-325-5p mimic. Cell proliferation significantly increased, and inflammation related protein level was inhibited in the miR-325-5p mimic group. MiR-325-5p was predicted to specifically combine with the HDAC3 3′UTR region using the targetscan. MiR-325-5p mimic significantly regulated HDAC3-wt activity and HDAC3 level was lower in the miR-325-5p mimic group. Furthermore, overexpressed HDAC3 reversed miR-325-5p protecting effects on early brain injury (EBI) in SAH. Conclusions: MiR-325-5p targeted HDAC3 to protect early brain injury in SAH via NF-κB signal pathway.