ABSTRACT
OBJECTIVE@#To investigate the therapeutic effect of Epothilone D on traumatic optic neuropathy (TON) in rats.@*METHODS@#Forty-two SD rats were randomized to receive intraperitoneal injection of 1.0 mg/kg Epothilone D or DMSO (control) every 3 days until day 28, and rat models of TON were established on the second day after the first administration. On days 3, 7, and 28, examination of flash visual evoked potentials (FVEP), immunofluorescence staining and Western blotting were performed to examine the visual pathway features, number of retinal ganglion cells (RGCs), GAP43 expression level in damaged axons, and changes of Tau and pTau-396/404 in the retina and optic nerve.@*RESULTS@#In Epothilone D treatment group, RGC loss rate was significantly decreased by 19.12% (P=0.032) on day 3 and by 22.67% (P=0.042) on day 28 as compared with the rats in the control group, but FVEP examination failed to show physiological improvement in the visual pathway on day 28 in terms of the relative latency of N2 wave (P=0.236) and relative amplitude attenuation of P2-N2 wave (P=0.441). The total Tau content in the retina of the treatment group was significantly increased compared with that in the control group on day 3 (P < 0.001), showing a consistent change with ptau-396/404 level. In the optic nerve axons, the total Tau level in the treatment group was significantly lower than that in the control group on day 7 (P=0.002), but the changes of the total Tau and pTau-396/404 level did not show an obvious correlation. Epothilone D induced persistent expression of GAP43 in the damaged axons, detectable even on day 28 of the experiment.@*CONCLUSION@#Epothilone D treatment can protect against TON in rats by promoting the survival of injured RGCs, enhancing Tau content in the surviving RGCs, reducing Tau accumulation in injured axons, and stimulating sustained regeneration of axons.
Subject(s)
Animals , Rats , Disease Models, Animal , Epothilones , Evoked Potentials, Visual , Nerve Regeneration/physiology , Optic Nerve Injuries/metabolism , Rats, Sprague-Dawley , Retinal Ganglion Cells/physiologyABSTRACT
Objective To observe the effects of hyperbaric oxygen in the treatment of the rats with optic nerve crush. Methods In this study, 24 rats with traumatic optic nerve injury were recruited. The rats'left eyes were injured in the optic nerve and the right eyes as the controls were applied with sham-operation. The rats were divided into the treatment group and the control group in accordance with the random number table. The experimental group was treated with two-course hyperbaric oxygen one hour a day, 10 days a course. The control group breathed fresh air under standard atmospheric pressure. F-VEP was detected on day 3, 10, 20 during the experiment. Results In the control group, latency of F-VEP delayed (P＜0.05) and the amplitude of P100 decreased (P＜0.05) in the injured eye compared to the normal eye. In the experimental group, no obvious difference was found in the latency of F-VEP and the amplitude of P100 in the injured eye compared to the normal eye (P＞ 0.05) . The comparison of F-VEP data of the injured eyes showed that incubation period was in advance (P＜ 0.05) and amplitude increased (P＜0.05) in the experimental group. The comparison of F-VEP data tested at different time points was statistical significant. Conclusion The rat model of optic nerve injury was successful. Hyperbaric oxygen therapy showed no interference with the F-VEP data of the injured eye by causing no damage to the normal eye and was proved effective. Longer treatment provided better results.
ABSTRACT
Oncomodulin (OM) is known by us progressively as a Calcium binding protein.Recently, OM has been found that it is secreted by inflammatory cells (neutrophilic granulocyte), and a signal which can promote cell growth between innate immunity and neurons, and a key to regenerate the damaged optical nerves by activating inflammation.The function of promoting the regeneration progress of axons has become a hot issue in recent years.This article summarized the mechanism of OM and the relationship between inflammation-induced OM and optic nerve regeneration research and progress were reviewed.