Study of thioredoxin antioxidative system in lateral geniculate body of chronic intraocular hypertension rat

Abstract

To investigate the dynamic changes and molecular mechanisms of thioredoxin system in lateral geniculate body of chronic intraocular hypertension rats. Glaucoma model was established by cauterizing rat's episclera veins. Right eye is the treatment group, while left eye is the sham operation group, vein of which is just isolated not be cauterized. There were 25 rats in high intraocular pressure group, and 4 rats in control group. The expression of Trx, Trx1, Trx2, Sesn2, Srxn1, Txnip was detected by Western blot and RT-PCR at different time points after intraocular pressure rose (1, 3, 7, 14, 28 d), and were grouped according to the time points. Paired t test was used in the data analysis within each time group and one-way ANOVA was used in the comparisons among different time groups. After 3 days of glaucoma induction, the gray-scale value of thioredoxin (0.83 ± 0.02) was statistically significant decreased (F = 4.871, P = 0.005), compared with the control group (1.02 ± 0.04). After 14 days, TRX1 related expression level reduced to 0.63 ± 0.04, while the control group level was 0.96 ± 0.03 (t = 13.647, P < 0.05). The related expression level of SESN2 was 0.53 ± 0.11, but the control group expression was 0.96 ± 0.03 (t = 13.812, P < 0.05). SRXN1 decreased to 0.71 ± 0.05 and 0.49 ± 0.03 after 7 days and 14 days respectively, while the expression of control group were 0.97 ± 0.02 and 0.96 ± 0.02 respectively. (Group 7 d, t = 9.451, P < 0.05; group 14 d, t = 13.611, P < 0.01).On the contrary, expression of TXINP was upregulated to 1.83 ± 0.04 and 2.37 ± 0.03 respectively, while the expression of control group were 1.00 ± 0.02 and, 0.95 ± 0.03 (Group 7 d, t = 7.924, P < 0.05;14 d t = 12.637, P < 0.01) respectively. Oxidative stress existed in lateral geniculate body of chronic intraocular hypertension rat model, and the down-regulated expression of Trx, Trx2 of the Trx system in lateral geniculate body was inhibited by multiple pathways when oxidative damage occurs. The inhibitor genes on up-stream increased while promoting genes diminished.