Objective: To investigate the protective effect and mechanism of miRNA-29c in rat cerebral ischemia-reperfusion nerve injury.
Methods: Forty-eight male SD rats were randomly divided into sham operation group, model group, miR-29c NC group, and miR-29c inhibitor group. Except for the sham operation group, the other three groups were all tethered to establish the middle cerebral artery of rats. The focal ischemia-reperfusion injury model was established, and the neurobehavioral changes in the rats were evaluated 24 hours after the operation. The volume of the cerebral infarction, the apoptosis of the ischemic brain tissue, the expression of miR-29c in the brain tissue, and the superoxide Substance dismutase (SOD) activity, malondialdehyde (MDA) content, cysteine-containing caspase 3 (Caspase 3), Caspase 8 and Caspase 9 activities, and Bcl-2, Bax, Bak1, cleaved caspase 3, cleaved caspase 8 and cleaved caspase 9 protein expression.
Results: Compared with the sham operation group, the expression of miR-29c in the model group and the miR-29c NC group was significantly increased, the neurobehavioral score of the rats was increased, the volume of cerebral infarction was increased, the apoptosis rate was increased, the activity of SOD was decreased, the content of MDA, The activities of Caspase 3, Caspase 8 and Caspase 9 were increased, the expression of Bcl-2 was decreased, and the expressions of Bax, Bak1, cleaved caspase 3, cleaved caspase 8 and cleaved caspase 9 were increased, and the differences were statistically significant (P<0.01). Compared with the model group and miR-29c NC group, the miR-29c inhibitor group had significantly lower miR-29c expression, lower neurobehavioral score, lower cerebral infarction volume percentage, lower cell apoptosis rate, higher SOD activity, MDA content, The activities of Caspase 3, Caspase 8 and Caspase 9 were decreased, the expression of Bcl-2 was up-regulated, and the expressions of Bax, Bak1, cleaved caspase 3, cleaved caspase 8 and cleaved caspase 9 were down-regulated, and the differences were statistically significant (P<0.01).
Conclusion: miR-29c has a protective effect on cerebral ischemia-reperfusion injury in rats, which is related to improving the antioxidant capacity and regulating the expression of apoptosis-related proteins.