动物实验,miRNA-29c z-bo 2020-08-27 549

　　Objective: To investigate the protective effect of miRNA-29c on cerebral ischemia-reperfusion nerve injury in rats and its mechanism.

　　Methods: Forty-eight male SD rats were randomly divided into sham operation group, model group, miR-29cNC group, miR-29 inhibitor group, and sham operation group. The other 3 groups were all focal ischemic rats. The perfusion injury model is used to establish cerebral arteries, and evaluate the neurobehavioral changes of rats, cerebral infarction volume, cells in focal cerebral ischemia tissue, cell apoptosis, miR-29c expression and superoxide in brain tissue 24 hours after surgery . Dismutase (SOD) activity, malondialdehyde (MDA) content, cysteine-containing aspartate proteolytic enzyme 3 (Caspase3), Caspase8 and Caspase9 activities, Bcl-2, Bax, Bak1, cleavedcaspase3, cleavedcaspase8 and Expression of cleavedcaspase9 protein.

　　Results: Compared with the sham operation group, the expression of miR-29c in the model group and the miR-29cNC group increased significantly, the neurobehavioral score of rats increased, the number of cerebral infarctions increased, and the rate of apoptosis was higher. SOD activity increased, decreased, MDA content increased, Caspase3, Caspase8, Caspase9 activity, inhibited Bcl-2 expression, inhibited Bax, Bak1, cleavedcaspase3, cleavedcaspase8, cleavedcaspase9, the difference was statistically significant (P\u003c0.01). Compared with the model group and the miR-29cNC group, the miR-29c expression in the miR-29 inhibitor group was significantly reduced, the neurobehavioral score of rats was reduced, the percentage of cerebral infarction volume was reduced, and the apoptosis rate was reduced. Decrease, SOD activity increased, MDA content, Caspase3, Caspase8 and Caspase9 activity decreased, Bcl-2 expression was up-regulated, Bax, Bak1, cleavedcaspase3, cleavedcaspase8, cleavedcaspase9 expression was down-regulated, and the difference was statistically significant (P\u003c0.01).

　　Conclusion: miR-29c has a protective effect on cerebral ischemia-reperfusion nerve injury in rats, and is related to the increased antioxidant capacity and the regulation of the expression of apoptosis-related proteins.