Abstract
ObjectiveTo investigate the effect of molecular hydrogen (H2) in a rat model subjected to optic nerve crush (ONC).MethodsWe tested the hypothesis that after optic nerve crush (ONC), retinal ganglion cell (RGC) could be protected by H2. Rats in different groups received saline or hydrogen-rich saline every day for 14 days after ONC. Retinas from animals in each group underwent measurements of hematoxylin and eosin (H&E) staining, cholera toxin beta (CTB) tracing, gamma synuclein staining, and terminal deoxynucleotidyltransferase-mediated dUTP nick end labeling (TUNEL) staining 2 weeks post operation. Flash visual evoked potentials (FVEP) and pupillary light reflex (PLR) were then tested to evaluate the function of optic nerve. The malondialdehyde (MDA) level in retina was evaluated.ResultsH&E, gamma synuclein staining and CTB tracing showed that the survival rate of RGCs in hydrogen saline-treated group was significantly higher than that in saline-treated group. Apoptosis of RGCs assessed by TUNEL staining were less observed in hydrogen saline-treated group. The MDA level in retina of H2 group was much lower than that in placebo group. Furthermore, animals treated with hydrogen saline showed better function of optic nerve in assessments of FVEP and PLR.ConclusionThese results demonstrated that H2 protects RGCs and helps preserve the visual function after ONC and had a neuroprotective effect in a rat model subjected to ONC.
Highlights
Traumatic optic neuropathy (TON) is one of the most devastating causes of permanent visual loss and blindness [1]
The number of surviving retinal ganglion cell (RGC) was assessed by anterograde tracer FITC-conjugated cholera toxin B (CTBFITC)
More gamma synuclein stained RGCs were observed in the H2 saline group than that in the placebo group demonstrating statistically significant difference between the survival rate of two groups (21.4463.48 cells/HPF versus 15.5062.09 cells/HPF; p, 0.01; Fig. 3D).The results showed that the RGC survival rate was higher in the H2 saline group than that in the placebo group, which morphologically indicated that the H2 saline had a significant neuroprotective effect on rat’s optic nerve after optic nerve crush (ONC)
Summary
Traumatic optic neuropathy (TON) is one of the most devastating causes of permanent visual loss and blindness [1]. Previous studies demonstrated that there are commonly two pathophysiology processes shared by retinal ganglion cells (RGCs) after optic nerve crush (ONC) [2,3], which are necrosis and apoptosis. In 1999, Bien et al found that after partial optic nerve injury, a fraction of RGCs underwent early necrosis, whereas others were subjected to delayed apoptotic death in the initial phase of RGC degeneration [2]. RGCs apoptosis was observed for up to 6 weeks, with most apoptotic cells in the first 2 weeks after ONC. Though research in this area is substantial, the specific mechanism underlying neural degeneration after ONC is not fully understood. Oxidative stress is considered as one of the most important factors that mediate the process of apoptosis [4,5]
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