| Objective: Optic nerve damage can lead to vision loss and blindness, early drug application is still the main method. Taurine is a type of sulfur-containingβ-amino acids, may be as a neurotransmitter or regulate substances playing a relevant role in the central nervous systemthe. The prective effect of nerve is achieved by preventing lipid peroxidation. Taurine can against a certain resistance to apoptosis in the role of genes, by means of anti-oxidant to protect cells from oxidative injury to achieve the anti-apoptosis. Taurine has been applied to many aspects of clinical, but has not been used in the optic nerve injury in vivo. In this study, mis-classification damage analogue of rats were made, and given taurine by intraperitoneal injection.At 3,7,14,28day after the optic nerve injury, the retinal morphology changes and the nitric oxide synthase (iNOS) changes in the optic nerve were observed. At the same time, the activity of superoxide dismutase (SOD) and the content of malondialdehyde aldehyde (MDA) were determined. We expected that this research would provide experimental evidence and theoretical basis of taurine in the treatment of optic nerve injury.Methods:84 female SD clean grade rats, weighing 250g±10g, with no pathological changes by examination of fundus and outer eye, were included in the experiment. Made 4 goups according to random check list, normal group (12 rats), control group (24 rats), treatment group (24 rats), pretreatment group (24 rats). The control group, treatment group and pretreatment group of 72 rats were made mis-classification damage analogue with right eye and not do processing with left eye, normal group received no treatment. After 1 hour from injury, rats of the control group were given distilled water (at 250mg/kg dose) by intraperitoneal injection once a day until the end of the experiment. At the same time, rats of the treatment group were given taurine (The taurine medicinal powder matches 5% densities with the distilled water, 200 items filter the membrane filtration to eliminate the fungus reserve to use) by intraperitoneal injection once a day until the end of the experiment. 3 days before injury rats of the pretreatment group were given taurine (dose, concentration and method as the same with the treatment group) once a day until the end of the experiment. At 3 days, 7 days, 14 days, 28 days after injury, the double eyeball of 3 normal group rats and the right eye of 6 rats in the other group were excised. Taken the optic nerve and retina tissue to be observed. The morphologic changes of the retina were observed by HE staining, the optic nerve tissue of nitric oxide synthase (iNOS) positive cells optical microscopy were observed by immunohistochemistry. Using the method of xanthine oxidase to detect the superoxide dismutase (SOD ) activity and the improved thiobarbituric acid (TBA) fluorometric to detect the malondialdehyde (MDA) content in optic nerve. The data were expressed by the x±s. Statistics analysis were used by analysis of variance and SPSS 13.0 software package.Results:1 Through HE staining ,normal retinal ganglion cell layer, inner nuclear layer and photoreceptor cell layer of the structure was clearly .The retinal ganglion cells (RGCs) of control group were disordered at every time points, showing vacuolization of the RGCs, inner nuclear layer and the varying degrees of reduction of photoreceptor cell. The above changes could also be found in the treatment group, but was lighter damage than that of control group. At the different experiment time points, there was no significant difference between the the pretreatment group and treatment group.2 There was few of iNOS masculine cells expresssion in normal group. In entire experiment process, the iNOS masculine cell changed had not been obviously, the expression was in the low level, but the grey level was high. At 3 days iNOS masculine cell of control group increased, the grey level droped, 7 days droped reach the peak, 14 days had the trend of escalation, 28 days continue to rise. At 3 days iNOS masculine cell of treatment group iNOS masculine cell grey level peak was not obvious, 3 days droped, continue to 7 days, 14 days droped reach the peak, until 28 days. At 3 days iNOS masculine cell of pretreatment group iNOS masculine cell grey level started to drop, 7 days to 14 days droped slowly, 14 days to 28 days droped obviously.At the experiment 3 days, 7 days, 14 days and 28 days, in control group and pretreatment group, the gray value of iNOS-positive cells in the optic nerve was significantly lower than that of in the normal group (P <0.01). The gray value of iNOS-positive cells in the treatment group was higher than that of in the normal group (14 days P <0.05,3-day, 7 days and 28 days, P <0.01), with statistical significance. It was significantly higher in the treatment and pretreatment group than the control group (P <0.01), with a very significant difference. At 3 day, the gray value of iNOS-positive cells in optic nerve in treatment group was higher than that of in the pretreatment group (P <0.05). At 7 days, 14 days, 28 days, there was no significant difference between that of in the treatment group and in the pretreatment group (P> 0.05).3 In the normal group, the expression of SOD activity in optic nerve was in a high level, no obviously change in the period of the experment. In the control group, the SOD activity of optic nerve organization droped from 3 day to 28 days, in 7 days and 14 days droped obviously. In the treatment group, the SOD activity droped at 3 days, 7 days droped not obviously, until 28 days. In the pretreatment group, the SOD activity of optic nerve organization droped not obviously at 3 days, 7 days drops, until 28 days. At the experiment 3 days, 7 days, 14 days, 28 days in control group, treatment group, SOD activity expression in the optic nerve was significantly lower than the normal group (P <0.01), with a very significant difference. The pretreatment group at different time points SOD activity in the optic nerve was lower than the same period in the normal group (3 days P <0.05,7 days, 14 days, 28 days P <0.01), all with statistical significance. At different time points the optic nerve SOD activity in the treatment group and pretreatment group was significantly higher than the control group (3 days, 7 days, 14 days, 28 days all P <0.01), with a very significant difference. At 3 day the optic nerve expression of SOD activity in treatment group was lower than the same period in pretreatment group (P <0.05), with statistical significance. Treatment group at 7 days, 14 days, 28 days, SOD activity in the optic nerve was no significant difference with the pretreatment group (P> 0.05).4 To the MDA content of optic nerve organization,there was no obviously change in the normal group, it expression was in the low level. In the control group, the MDA content of optic nerve organization elevated at 3 days, 7 days and 14 days elevated obviously, 28 days continue to elevate. In the treatment group, the MDA content of optic nerve organization elevated at 3 days, 7 days elevated obviously, later elevated slowly, until 28 days. In the pretreatment group, the MDA content of optic nerve organization elevated not obviously at 3 days, 7 days elevated, until 28 days. At the experiment 3 days, 7 days, 14 days, 28 days MDA content in the optic nerve in control group, treatment group, was higher than in normal group (P <0.01), with a very significant difference. MDA content of the pretreatment group at different time points expressed higher than the normal group (3 days P <0.05,7 days, 14 days, 28 days P <0.01), with statistical significance. At different time points MDA content in the optic nerve of treatment group and pretreatment group was significantly lower than that of the same period in the control group (3 day, 7 days, 14 days, 28 days all P <0.01), with a very significant difference. MDA content in the optic nerve of treatment group at 3 day expressed higher than that of the corresponding pretreatment group (P <0.05), with statistical significance. MDA content in the optic nerve of treatment group at 7 days, 14 days, 28 days expressed no significant difference with pretreatment group at the same period (P> 0.05).Conclusions:1 After traumatic optic nerve injury, the RGCs and nerve fibers were irregularly arranged, cell numbers were reduced.2 Taurine could reduce nitric oxide synthase (iNOS) expression, increase superoxide dismutase (SOD) activity, reduced malondialdehyde (MDA) content in the optic nerve tissues after traumatic optic nerve injury. 3 Taurine can reduce RGCs and optic nerve damage after traumatic optic nerve injury, and has some protective effects to the optic nerve. |
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