ABSTRACT
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.
ABSTRACT
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.
ABSTRACT
Background Radiation-induced optic neuropathy (RION) is a severe complication after radiotherapy for head and neck cancer,which threatens the visual acuity and quality of life of patients.Till now,there is no recognized treatment for RION.It is of great significance to study the natural progression of the RION,and to prevent and treat RION.Objective This study was to establish an ideal radioactive optic nerve injury animal model.Methods Healthy 8-week SD rats with hygiene grade were randomly divided into normal control group and model group,with 6 rats in each group.The total 30 Gy dose of radiation with 3 portions was used to irradiate the head model group rats;ELISA was performed to analysis the changes of endothelin-1 (ET-1) and Von Willebrand factor (vWF) concentrations in blood 2,4 and 8 weeks after irradiation.Hematoxylin-eosin staining and transmission electron microscope were performed to observe the changes of optic structure.The use and care of the experimental animals complied with the ARVO statement.Results The concentrations of ET-1 in the model group were (23.18± 0.11),(27.98 ±0.22),(33.90 ±0.1 1),(65.25 ±0.38) and (43.82 ± 0.09) pg/ml before irradiation,1 day,2,4,6 weeks after irradiation,those in the normal control group were (22.65 ± 0.14),(23.18 ± 0.19),(23.68 ± 0.15),(24.23±0.12) and (23.58±0.16)pg/ml.The concentrations of vWF in the model group were (63.16±2.21),(88.32± 2.06),(123.38 ± 1.36),(191.40 ± 0.61) and (141.69 ± 0.82) pg/ml before irradiation,1 day,2,4,6 weeks after irradiation,those in the normal control group were (62.82 ± 1.56),(63.35 ±2.06),(64.12 ± 1.76),(63.52±2.02) and (63.48 ± 1.55)pg/ml.There were significant differences of ET-1 and vWF concentrations among different groups and time points (ET-1:Fgroup =32.160,P =0.012;Ftime =21.180,P =0.023.vWF:Fgroup =73.110,P=0.001;Ftime =46.180,P =0.002).The nerve fiber bundles was swelled with disordered arrangement and vacuolization 8 weeks after irradiation.Axon swell and atrophy,axons with myelin sheath layer plate separation were obtained.The rates of axon demyelination in the normal control group and model group were (1.35 ±0.79) ％ and (14.44±2.32)％,respectively.There was a statistically significant difference between the two groups (t =14.07,P＜0.01).Conclusions The total 30 Gy dose of radiation on the head of rats can make stable radioactive optic nerve injury model.This model making method is simple,cheap and practical,which is worth further study.
ABSTRACT
Objective To observe the concentration of plasma endothelin (ET-1) in patients with nonarteritic anterior ischemic optic neuropathy(NAION) and investigate the relationship between ET-1 and NAION. Methods The plasma levels of ET-1 in 41 patients with NAION and 15 age-matched normal control subjects were measured by radioimmuoassay (RIA). The patients with NAION were divided into high papilloedema group, light papilloedema group, and recovery group according to the degree of papilloedema; and were divided into group1 (within 14 days), 2 (within 15-30 days), 3 (within 31-60 days), and 4 (within 61-180 days) according to the disease course. The plasma levels of ET-1 in different groups were detected and compared. Results The plasma level of ET-1 in patients with NAION was significantly higher than that in the normal subjects ( t=5.02,P