| Traumatic optic neuopathy which is one of the common kinds of ocular trauma often results in sever vision deterioration even permanent blindness. Many factors including deprevivation of nerve growth factors, the calcium overload and free radicals can change the RGC microenviroment after optic nerve injury. The research of nerve protection drugs curing optic injury is still in animal experimental stage. High dose corticosteroid is the common therapeutic method in recent years. High dose corticosteroid is used to treat with traumatic optic neuopathy, beacause it can cure acute spinal cord injury. Methylprednisolone is used not as widely as dexamethasone(DX)because of its higher price .In the study , the modle of optic nerve crush was established and given high dose DX at the early stage . Biochemical assays, morphological observation and TUNEL technique were used to investigate the therapeutic effect and mechanism.Materials and methodOne hundred and four healthy adult Wistar rats without eye diseases were divided into three groups randomly: normal control group(n=8,16eyes), crush control group(n=48, 48eyes)and treatment group(n=48, 48eyes). According to the surviving time after crush , the groups were sub-divided into 3 timepionts: 4d, 7d and 14d, thereare 16 eyes at each timepiont in each group. The animal of the crush group and treatment group received optic nerve crush in unilateral eye by applying the lips of a cross-action forceps to the nerve at 3mm behind the globe for 12s. The treatment group were given DX 0.25mg/kg/6h from 1 h post-crush to 48h. Crush control group received equal volume normal saline. All animals were sacrificed respectively at 4d, 7d and 14d after optic nerve crush, and the eyes were encleated. The morphologic chang of retina was studied by light microscopy and RGC was caculated. Retina was taken out and homogenized in order to measure the activity of Na+-K+-ATPase and the content of malonyldialohyed(MDA). The apoptosis cell of retina was examined by Terminal deoxynudeotidyl trasferase TDT - mediated dUTP - biotin nick end labeling (TUNEL)reaction .All the data were analyzed statistically by ANOVA and independent-sample / test. Result1 .HE stain showed: HE stain indicated the gradual loss of cell nuclear in the ganglion cell layer and the continous atrophy of the nerve fiber layer , inner nuclear layer and outer nuclear laye in crush-control group . Nuclear densification was observed 7days after crush and still exist 14 days after crush. While the pathelogical changes were remarkablly alleviated after treating with high dose DX. Got the average number of RGC per X 200 visual field , in normal control group, the number was 30.500; in crush control group.the number were30.125, 21.125, 12.125 at 4d, 7d and 14d post -crush, respectively; in treatment group , the number were30.75, 24.875, 20.125, respectively. High dose DX significantly protected the RGC (P<0.05)at various tune points.2 .Content of MDA: the content of MDA in normal group was 3.597 nmol/mg prot; in crush control group , the content of MDA were 5.368 nmolAng prot, 7.070 nmol/mg prot, 12.044 nmol/mg prot at 4d, 7d and 14d post -crush, respectively; in treatment group, the content of MDA were 3.808 nmol/mg prot, 4.639 nmol/mg prot, 7.349 nmol/mg prot at 4d, 7d and 14d post -crush respectively. The content of MDA in crush control group was higher than the normal control group and lower than the treatment group at each timepiont (P<0.05).3. Activity of Na+-K+-ATPase; the activity of Na+-K+-ATPase in normal control group was 6.077 umolpi/mgprot/hour; in crush control group , the activity of Na+-K+-ATPase were 4.642 umolpi/mgprot/hour , 2.192 umolpi/mgprot/hour ,1.372 umolpi/mgprot/hour at 4d, 7d and 14d post -crush ,respectively; in treatment group , the activity of Na+-K+-ATPase were 4.834 umolpi/mgprot/hour , 3.025 umolpi/mgprot/hour , 1.973 umolpi/mgprot/hour at 4d, 7d and 14d in post -crush , respectively. The activity of Na+-K+-ATPase in crush control group was lower than the normal control group and the tr... |
PDF Full Text Request