The mice in the KA group developing acute seizure were further subjected to intracerebroventricular injection (i.c.v.) of antagomir negative control (NC) or miR-155 antagomir.
The expression of TNF-α reached peak levels in the acute phase (2h post-SE) of seizure and then gradually decreased; however, it rose again in the chronic phase (60 days post-SE). miR-155 expression started to increase 2 h post-SE, reached peak levels in the latent phase (7 days post-SE) of seizure and then gradually decreased.
In addition, rno-miR-155-5p as well as rat Sestrin-3 mRNA and protein expression were partly dependent on oxidative stress induced by H<sub>2</sub>O<sub>2</sub> in PC12 cells<sub>.</sub> Taken together, our data suggest that rno-miR-155-5p is a potent post-transcriptional regulator of rat Sestrin-3 and it may be one of the molecular links between brain damage and increased risk for seizures during damage by oxidative stress.
RT‑qPCR analysis indicated that miR‑155 levels in patients who experienced seizures increased 2.45‑fold compared with patient who did not experience seizures, indicating miR‑155 may be a potential biomarker for the occurrence of seizures.