Effect of inhibition of immunosuppressive factor COX-2 on apoptosis of retinal ganglion cells and regulation of p38MAPK signal pathway / 中国免疫学杂志

Objective: To investigate the effect of COX-2 inhibitor bevacizumab on the activity and apoptosis of retinal ganglion RGC-5 cells induced by H2O2 and the regulation of p38 MAPK signaling pathway. Methods: Retinal ganglion RGC-5 cells was stimulated using H2O2 ( 200, 300, 400, 600, 800 μmol/L) to establish a H2O2 damage model, H2O2 concentration was selected based on half inhibitory concentration, COX-2 inhibitor bevacizumab treated RGC-5 cell induced by H2O2 for 7 h, SB203580 as a p38 MAPK signaling pathway inhibitor, cell viability and apoptosis rate were detected by MTT method and flow cytometry, respectively; the expression of PCNA, p53, p38 and p-p38 protein were detected by Western blot. Results: Different concentrations of H2O2 could inhibit the viability of RGC-5 cells, and the cell viability decreased with the increase of H2O2 concentration, because 400 μmol/L H2O2 inhibited half of the cell viability, it was selected as an object of study. Compared with the control group, the cell viability and the expression of PCNA were decreased significantly in H2O2 group, the apoptosis rate and the expression of p53 and p-p38 protein was increased significantly; compared with H2O2 group, the cell viability and PCNA expression were increased significantly in the H2O2+bevacizumab group, the apoptosis rate and the expression of p53 and p-p38 protein were decreased significantly ( P ＜ 0. 05); compared with H2O2+ bevacizumab group, the cell viability and PCNA expression were increased significantly in H2O2+bevacizumab+SB203580 group, the apoptosis rate and the expression of p53 and p-p38 protein were decreased significantly ( P＜0. 05). Conclusion: Inhibition of immunosuppressive factor COX-2 expression can improve the activity of retinal ganglion cells and inhibit apoptosis by regulating the p38 MAPK signaling pathway.

Cultured human embryonic neocortical cells survive and grow in infarcted cavities of adult rat brains and interconnect with host brain / 中华医学杂志(英文版)

<p><b>BACKGROUND</b>There are no reports on exnografting cultured human fetal neocortical cells in this infracted cavities of adult rat brains. This study was undertaken to observe whether cultured human cortical neurons and astrocytes can survive and grow in the infarcted cavities of adult rat brains and whether they interconnect with host brains.</p><p><b>METHODS</b>The right middle cerebral artery was ligated distal to the striatal branches in 16 adult stroke-prone renovascular hypertensive rats. One week later, cultured cells from human embryonic cerebral cortexes were stereotaxically transferred to the infarcted cavity of 11 rats. The other 5 rats receiving sham transplants served as controls. For immunosuppression, all transplanted rats received intraperitoneal injection of cyclosporine A daily starting on the day of grafting. Immunohistochemistry for glial fibrillary acidic protein (GFAP), synaptophysin, neurofilament, and microtubule associated protein-2 (MAP-2) was performed on brain sections perfused in situ 8 weeks after transplantation.</p><p><b>RESULTS</b>Grafts in the infarcted cavities of 6 of 10 surviving rats consisted of bands of neurons with an immature appearance, bundles of fibers, and GFAP-immunopositive astrocytes, which were unevenly distributed. The grafts were rich in synaptophysin, neurofilament, and MAP2-positive neurons with long processes. The graft/host border was diffuse with dendrites apparently bridging over to the host brain, into which neurofilament immunopositive fibers protruded.</p><p><b>CONCLUSION</b>Cultured human fetal brain cells can survive and grow in the infarcted cavities of immunodepressed rats and integrate with the host brain.</p>