动物造模,大鼠脑缺血再灌注神经损伤 z-bio 2021-07-16 643

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

　　Method: 48 male SD rats were randomly divided into sham operation group, model group, miR-29cNC group and miR-29 inhibitor group. The other 3 groups were medium except for sham operation group. Used to establish cerebral arteries. The rat model of ischemia-reperfusion injury was used to evaluate the neurobehavioral changes of rats 24 hours after surgery. Detect cerebral infarction volume, cell apoptosis, brain tissue miR-29c expression, and superoxide on the ischemic side. Dismutase (SOD) activity, malondialdehyde (MDA) content, cysteine-containing aspartate proteolytic enzyme 3 (caspase 3), caspase 8 and caspase 9 activities, and Bcl-2, Bax, Bak1 Expression of cleavedcaspase3, cleavedaspase8 and cleaved caspase9 proteins.

　　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 volume of cerebral infarction increased, the rate of apoptosis increased, and the activity of SOD increased. MDA content decreased, caspase 3, caspase 8 and caspase 9 activities increased, Bcl-2 expression was down-regulated, Bax, Bak1, cleavedcaspase3, cleavedcaspase8 and cleavedcaspase9 were up-regulated, and the difference was statistically significant (Pu003c0.01). Compared with the model group and miR-29cNC group, the expression of miR-29c 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 significantly reduced. high. It dropped. SOD activity increased, MDA content decreased, caspase 3, caspase 8 and caspase 9 activity, Bcl-2 expression was up-regulated, Bax, Bak1, cleavedcaspase3, cleavedcaspase8 and cleavedcaspase9 expression was down-regulated, the difference was statistically significant (Pu003c0.01).

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