BACKGROUND:Studies have shown that neural stem cells isolated from embryonic rat cerebral cortex can proliferate and differentiate into neurons, astrocytes and oligodendrocytes in col agen gels.
OBJECTIVE:To investigate the effect of neural stem cells combined with col agen gel on the apoptosis of nerve cells in the brain of rats after spinal cord injury.
METHODS:Forty-five spinal cord injury rat models were made through spinal cord hemisection and randomly divided into three groups. At 1 week after modeling, rats in the celltransplantation group were injected al ogeneic neural stem cellsuspension into the injured site, rats in the combination group were administered with al ogeneic neural stem cells/col agen gel suspension into the injured site, and rats in the model group received no treatment. RESULTS AND CONCLUSION:From 1 to 8 weeks after injury, the Basso, Beattie and Bresnahan (BBB) locomotion scores in the combination group were significantly higher than those in the other two groups (P<0.05). Hematoxylin-eosin staining showed that at 1 week after transplantation, there were a few necrotic cells and Bcl-2 positive cells, but a large amount of Bax positive cells in the three groups. Then, the number of Bax-and Bcl-2-positive cells was reduced gradual yin the three groups. At 8 weeks after transplantation, the number of Bax-positive cells was significantly higher in the model group than the other two group (P<0.05), but the number of Bcl-2-positive cells were dramatical y lower (P<0.05). Meanwhile, there were no necrotic cells in the three groups. These findings indicate that neural stem celltransplantation combined with col agen gel scaffold can arrest apoptosis of nerve cells in the brain of rats after spinal cord injury, and promote functional recovery after spinal cord injury.

Purpose: Cervical cancer is one of the most fatal diseases among women in under-developed countries. To improve cervical cancertreatment, discovery of new targets is needed. In this study, we investigated the expression of NUP210, miR-22, and Fas in cervicalcancer tissues and their functions in cell cycle regulation. Materials and Methods: We detected and compared the expression levels of NUP210, miR-22, and Fas in cervical cancer tissueswith paired normal tissues using immunohistochemistry, Western blot, and real-time quantitative polymerase chain reaction.NUP210 was knocked down in HeLa cells via lentivirus, followed by cell cycle and proliferation analysis. Using a luciferase reporterassay, we explored the link between miR-22 and NUP210. We overexpressed miR-22 in HeLa cells and analyzed cell cycle and proliferationfunction. We then overexpressed miR-22 in NUP210 knockdown cells to explore the connection between Fas and miR-22-NUP210 signaling. Results: We found that NUP210 was overexpressed in cervical cancer patients. Knocking down NUP210 restored cell apoptosisand proliferation. We confirmed miR-22 as a regulator of NUP210 and verified that miR-22 was inhibited in cervical cancer development.We also found that restoring miR-22 expression could induce cell apoptosis. Finally, we found that miR-22-regulated expressionof NUP210 could alter Fas expression and, in turn, elicit cell cycle arrest and proliferation. Conclusion miR-22 in cervical cancer is downregulated, resulting in NUP210 overexpression and inhibition of Fas-induced cellapoptosis.