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[Experimental study on treatment of rabbits optic nerve injury with Caspase-3 inhibitor z-DEVD-fmk]
Wei Zhang1, Jin-guo Yu, Xing Wang
1Department of Ophthalmology, Tianjin Huan Hu Hospital, Tianjin 300060, China.
Objective:
To observe the effects of caspase-3 inhibitor z-DEVD-fmk on optic nerve injury of rabbits.
Methods:
It was an experimental study. Two to three month-old rabbits were used in this study. The rabbit model of optic nerve injury was created by fluid percussion brain injury device (FPI). DMSO (5 µl 2% solution) was injected intravitreally to the left eyes (control group). Caspase-3 inhibitor z-DEVD-fmk (5 µl) was injected intravitreally to the right eyes (experimental group). Flash-visual evoked potential (F-VEP) and histopathological examination of the retina were used to check the variations in optic nerve injury at 1, 4, 7, 10, 14, and 21 days after the treatment. Immunohistochemistry was used to detect the expression of caspase-3 in the retina. T-test, variance analysis, q-test and linear correlation analysis were used to analyze these data.
Results:
At the 7th day after treatment, the latency of F-VEP P1 in experimental group was shorter than that in the control group [(90.50±7.61) ms vs (113.59±12.92) ms, t=4.060, P<0.05] and the number of retinal ganglion cells (RGC) in the experimental group was greater than that in the control group (237.62±8.50 vs 207.03±11.04, t=-5.843, P<0.05). Both of these trends continued to the 21st day after treatment [(67.97±7.93) ms vs. (134.22±8.50) ms, t=13.950, P<0.05; 156.32±8.45 vs. 207.13±12.21, t=-10.307, P<0.05]. The absorbency (A) of caspase-3 in the experimental group (0.396±0.023) was lower than that in the control group (0.458±0.024) and this difference was statistically significant (t=6.200, P<0.05) at the 7th day after treatment. The latency of F-VEP P1 and the absorbency of caspase-3 in the retina were positively correlated with each other (r=0.95, P<0.05).
Conclusion:
z-DEVD-fmk is effective in treating rabbit optic nerve injury by inhibiting the expression of caspase-3 in the retina. It can promote the recovery of optic nerve function.
Insights
The caspase-3 inhibitor z-DEVD-fmk effectively treats optic nerve injury in rabbits by reducing caspase-3 expression and promoting optic nerve function recovery. This study demonstrates its therapeutic potential for optic nerve damage.
Area of Science:
- Ophthalmology
- Neuroscience
- Pharmacology
Context:
- Optic nerve injury is a significant cause of vision loss.
- Caspase-3 plays a crucial role in apoptotic cell death following optic nerve injury.
- Developing effective neuroprotective strategies is essential.
Purpose:
- To evaluate the therapeutic effects of the caspase-3 inhibitor z-DEVD-fmk on optic nerve injury in a rabbit model.
- To assess the impact of z-DEVD-fmk on optic nerve function and retinal cell survival.
- To investigate the inhibition of caspase-3 expression by z-DEVD-fmk.
Summary:
- Rabbits with optic nerve injury received intravitreal injections of either a caspase-3 inhibitor (z-DEVD-fmk) or a control vehicle.
- Flash-visual evoked potential (F-VEP) and retinal histopathology were used to evaluate optic nerve function and retinal ganglion cell (RGC) survival.
- Immunohistochemistry confirmed reduced caspase-3 expression in the experimental group.
Impact:
- z-DEVD-fmk treatment significantly improved optic nerve function, evidenced by shorter F-VEP latency.
- The inhibitor increased RGC survival compared to the control group.
- Results indicate that z-DEVD-fmk is a promising therapeutic agent for optic nerve injury by inhibiting caspase-3-mediated apoptosis.
