ObjectiveTo observe the protective effect of human umbilical cord blood stem cells (hUCBSC) transplantation on retinal ganglion cells (RGC) after optic nerve injury. Method48 adult Sprague-Dawley rats were randomly divided into group A and B, therefore 24 rats in each group. Calibrated optic nerve crush injury model was induced in the left eyes, the right eyes served as a control. Medicine was injected at seventh day after optic nerve injury. PBS was injected into the eyes of Group A rats by peribulbar injection. The hUCBSCs were injected into the eyes of Group B rats by peribulbar injection. Seven days before sacrifice, 5% fluorogold was injected into superior colliculi bilaterally. At 7, 14, 21, 28 days after labeled, retinal flat mounts were observed under fluorescence microscope and optical microscope to investigate the morphological and RGC changes in density during retinal degeneration. ResultsThe RGC number showed a tendency to decline gradually along with increases of the time in two groups, but the trend of decrease of Group B was evidently slower than that of Group A. The RGC number of the injury eye were less than the control eye in Group A and B (t=3.24, 3.15; P < 0.05). At 7, 14, 21, 28 days after labeled, the RGC number (t=4.78, 4.70, 3.98, 3.27; P < 0.05) and labeled RGC rate (t=4.39, 4.21, 4.36, 5.07; P < 0.05) in group B were more than those in group A. After optic nerve injury, there was karyopycnosis on ganglion cell layer of retina, thinning on each layer of retina, derangement of cell and decrease in RGC. There was different degree of the above change in different time after optic nerve injury. There were the swelling, the hemorrhage, derangement of spongiocyte and the denaturation like vacuole in the spot of optic nerve injury. Moreover, they were aggravating with increases of the time after optic nerve injury. There was no pathological changes in normal eyes. ConclusionThe hUCBSC can increase the survival rate of the RGC and can rescue and(or) restore the injujed RGC after transplanted into body of optic nerve crush rat model by peribulbar injection.
Ras homolog family (Rho)/ Rho-associated coiled-coil kinase (ROCK) signaling pathway widely exists in human and mammal cells, which is closely related to inhibition of repair after optic nerve damage. The expression level of Rho/ROCK signaling pathway-related proteins is up-regulated in glaucoma, and related with the death of retinal ganglionic cell (RGC) and the axon activity. ROCK inhibitors can protect the surviving RGC and promote axon extension with a dose-dependent manner. ROCK inhibitors also can inhibit glial scar formation, lower intraocular pressure and inhibit inflammatory response to some degrees. Rho/ROCK signaling pathway correlates with the optic nerve disease progression, and ROCK inhibitors hope to become a new therapeutic drug.