To explore the effect of miR-1 on neuronal apoptosis in rats with
stroke through the ERK signaling pathway. Methods. Forty male rats (180-220 g) were selected and randomly divided into the
sham, model, miR-1 inhibitor, and miR-1 mimic groups (10 rats per group) by average
body weight.
Cerebral ischemia/reperfusion (I/R) models were established using a modified middle cerebral artery wire
thrombosis (MCAO) method in rats in the model group, miR-1 inhibitor group, and miR-1 mimic group. After the successful model establishment, the miR-1inhibitor group and miR-1 mimic group were intravenously injected with miR-1 inhibitor and miR-1 mimic, respectively, once a day for 3 days. The
sham and model groups were given the same dose of
normal saline. TTC staining was applied to detect the
cerebral infarct size and calculate the
infarct volume. Histopathological changes in the hippocampus of rat brains were observed by HE staining. Flow cytometry was used to detect neuronal apoptosis in rat brains. The
mRNA expressions of miR-1, ERK1/2, Bcl-2, and Bax in rat brain tissues were determined by QRT PCR, and the
protein levels of ERK1/2, Bcl-2, Bax, and
caspase-3 were determined by Western blot analysis. Results. Compared with the
sham group, the neurological impairment score,
cerebral infarct size, and volume of rats in the model group were significantly increased (p < 0.05). Compared with the model group, the neurological impairment score,
cerebral infarct size, and volume were significantly increased in the miR-1 mimic group and significantly decreased in the miR-1 inhibitor group (p < 0.05). In the model group, the hippocampal tissue of rats had malaligned cells, neuron cell
atrophy became smaller, the intercellular spaces became larger, and vacuoles appeared. Compared with the model group, the miR-1 inhibitor group could effectively alleviate the pathological changes in the hippocampus, and the miR-1 mimic group could significantly add to the pathological changes in the rat hippocampus. Compared with the
sham group, the
mRNA expression of miR-1 and Bax in the brain of model rats increased significantly (p < 0.05), and the
mRNA expression of ERK1/2 decreased significantly; Compared with the model group, the miR-1 and Bax
mRNA expressions in the brain tissues of rats in the miR-1 inhibitor group were significantly decreased, the ERK1/2 and bcl-2
mRNA expressions were significantly increased, and the miR-1 and Bax
mRNA expressions in the brain tissues of rats in the miR-1 inhibitor group were significantly decreased, and the Bcl-2
mRNA expression was significantly increased (p < 0.05). Compared with the
sham group, neuronal apoptosis was increased in the brain tissues of rats in the model group and miR-1 mimic group. Compared with the model group, neuronal apoptosis was decreased in the brain tissues of rats in the miR-1 inhibitor group. Compared with the
sham group, the ERK1/2
proteins in the model group were significantly decreased, the Bcl-2, Bax, and
caspase-3 proteins were significantly increased, and the ERK1/2, Bcl-2, Bax, and
caspase-3 proteins in the miR-1 inhibitor group and miR-1 mimic group were significantly increased. Compared with the model group, the
protein levels of ERK1/2 and Bcl-2 in the miR-1 inhibitor group were significantly increased, the
proteins of Bax and
caspase-3 were significantly decreased, and the
protein levels of ERK1/2 and Bcl-2 in the miR-1 inhibitor group were significantly increased (p < 0.05). Conclusions. miR-1 can interfere with neuronal apoptosis in rats with
stroke through the ERK signaling pathway.