Objective:To explore the regulatory effect of miR-873-5p micro-RNA targeting voltage-dependent anion channel protein 1 (VDAC1) in neurons and its mechanism.Methods:Murine nerve cells were randomly divided in vitro into a control group, a model group, a mimetic negative carrier (miR-con) group and an miR-873-5p group. The epileptiform hippocampal nerve cell model was induced in all of the cells except those in the control group using magnesium-free medium. The control group was normally cultured, while the miR-con and miR-873-5p groups were transfected with miR control and miR-873-5p RNA respectively. Real-time fluorescent quantitative polymerase chain reactions were used to detect the expression of miR-873-5p and VDAC1 mRNA. Western blotting was employed to detect VDAC1, B-cell lymphoma/leukemia-2 protein (Bcl-2), Bcl-2 associated X protein (Bax) and cleared caspase-3 in the neurons. The levels of reactive oxygen species (ROS), malondialdehyde (MDA) and glutathione (GSH) were measured using the DCFH-DA fluorescent probe, the thiobarbituric acid method and enzyme-linked immunosorbent assay respectively. Any apoptosis was detected using flow cytometry, while the targeting of miR-873-5p on VDAC1 was verified using the double fluorescence zymase reporter gene method.Results:Compared with the control group, a significant decrease in the average expression of miR-873-5p, Bcl-2 and in GSH and MDA levels was observed in the model group, but there was a significant increase in the average level of VDAC1, Bax, cleaved caspase-3 and ROS and in the rate of apoptosis. Compared with the miR-con group, a significant decrease in the average expression of Bax, cleaved caspase-3, ROS and in the apoptosis rate was observed in the miR-873-5p group, but there was a significant increase in the average level of Bcl-2, GSH and MDA. Moreover, it was verified that miR-873-5p reduced the expression of VDAC1.Conclusion:miR-873-5p protects damaged neurons by inhibiting their apoptosis through negatively regulating the target gene VDAC1 and the oxidative stress response.

Objective To study the effects of enriched rehabilitative training on the expression of microtu-bule associated protein 2 (MAP-2) and synaptophysin (SYN), and to explore its relationship with brain plasticity. Methods Seventy-seven male Wistar rats weighing 160 to 200 g were randomly divided into an ischemia + enriched rehabilitation group (IE, n=36), an ischemia + standard rehabilitation group(IS, n=8), a sham ischemia + en-riched rehabilitation group (SE, n=21) and a sham ischemia + standard rehabilitation group (SS, n=12). Rats in the ischemia groups had their middle cerebral artery sutured for two hours before reperfusion, while those in the sham groups had a similar operation without occlusion. The enriched groups were given enriched rehabilitative train-ing, while the standard groups were left without any training. Behavioral tests, including the acrobatic performance, were administered once daily 2 days after operation, and SP staining of MAP2 and SYN were used to observe the func-tional recovery and brain plasticity changes among the groups at 1,7, 14, 21 and 28 days after the operations. Re-sults Acrobatic performance times reduced gradually. Bederson scores were significantly better in the IE than in the IS group by the 28th day after the operation). There was no significant difference between IE and IS groups in a foot fault test). The expression of MAP-2 and SYN around the infarct and in the hippocampus decreased significantly at first), then recovered gradually. The expression of MAP-2 and SYN in the IE group was significantly higher than that in the IS group at various time points of observation). Conclusion Enriched rehabilitative training can improve functional recovery and the expression of MAP-2 and SYN after brain ischemia, and the functional enhancement may attribute to the brain plasticity.