LAUSR

OBJECTIVE Cerebral hemorrhage can cause hemorrhagic stroke, leading to severe brain damage. MiRNA-155 is closely related to the development of stroke. However, the regulatory mechanism of miRNA-155 during cerebral ischemia has not yet been elucidated. MATERIALS AND METHODS SD rats were separated to sham operation group, model group, miRNA-155 inhibitor group and miRNA-155 agonist group followed by analysis of neural function, miRNA-155 and pacemaker ion channel hyperpolarization-activated, cyclic nucleotide-gated (HCN) expression by Real Time PCR. Meanwhile, Caspase 3 activity, glutamic acid (Glu) and γ-aminobutyric acid (GABA) content were also measured along with analysis of IL-6 and IL-1β secretion by ELISA as well as reactive oxygen species (ROS) content and superoxide dismutase (SOD) activity. RESULTS Compared to sham operation group, model group presented significantly elevated miRNA-155 level and Longa score, decreased HCN expression, elevated Caspase 3 activity and Glu content, and reduced GABA and SOD activity. Meanwhile, model group also had elevated IL-6 and IL-1β secretion, and ROS content (p<0.05). The miRNA-155 agonist group further exacerbated these changes (p<0.01). The miRNA-155 inhibitor group could inhibit miRNA-155 expression and significantly reverse the above pathological changes (p<0.05). CONCLUSIONS miRNA-155 is increased in cerebral ischemia. Regulation of miRNA-155 expression can target neuronal pacing ion channel HCN channel to regulate the release of amino acid transmitters, thereby alleviating the progress of cerebral ischemia.