| Objectives To observe the effect of nimodipine on the number of axons in optic nerve,the cell count of LGN neuron cells and the expression of Bcl-2,Bax and apoptosis in the lateral geniculate body caused by chronic ocular hypertension.Methods Choose 60 healthy male New Zealand white rabbits(provided by the animal experiment center of North China University of Science and Technology),randomly divided into normal(A)group(12),injury(B)group(24),treatment(C)group(24).The right eye was used as the experimental eye.Group A shall not be treated with special disposition,group B and C was made into chronic ocular hypertension model with compound carbomer.After the model was made successfully,the group C was fed nimodipine 13.2mg/kg(dissolved in sterilization injection water)1 times a day,group A and B was fed the same amount of physiological saline,continuously drench for 8 weeks.The white rabbits of each group were injected with 25% uratan general anesthesia in 2 weeks,4 weeks,6 weeks and 8 weekends.The blood-saline-formaldehyde replacement was completed by carotid perfusion,After the internal fixation was successful,open the skull,cut out the optic nerve about 3mm in length,and take out the entire brain tissue,fix the optic nerve and brain more than 48 h in paraformaldehyde.Take out the optic nerve and the lateral geniculate body tissue,embed them by paraffin,observe the number of axons in optic nerve of Nissl staining,the cell count of lateral geniculate nucleus of Nissl staining,the expression of Bcl-2 and Bax factor detected by immunohistochemistry,and the apoptotic expression detected by TENEL.Calculate the average optical density of positive expression in each group by Image-Pro Plus 6.0 optical density analysis software.Results 1 There was no statistically significant difference in the intraocular pressure of each group of white rabbits(P<0.05)before the ocular hypertension model was established.After the model was made successfully,there was no significant difference in intraocular pressure between group B and group C at the same time(P<0.05).It showed that the injection of compound carbomer can increase the intraocular pressure,and the treatment of nimodipine irrigation has no obvious effect on the intraocular pressure.2 Nissl staining The comparison of optic axon count per unit area between group B and group A was P<0.05,between group B and group C was P>0.05,At 8w,the optic axon count of group B was still further reduced(P<0.05),The comparison between group C and group A was P<0.05,This suggested that the optic axons were lost when the high intraocular pressure continued to 6w,and the axonal loss of the nimodipine treatment group appeared at 8w,indicating that nimodipine could delay the damage to a certain extent.The results of lateral geniculate nucleus were similar to those of the optic axons,showed that chronic ocular hypertension can directly damage optic nerve and upper lateral genicular neurons.3 Immunohistochemical staining There was only a small amount of Bcl-2 and Bax expression in the lateral geniculate nucleus of group A.The positive expression of Bcl-2 was increased from 4W in group B and C,maintain to 8w,the comparison of three time points in the group was statistically significant(P<0.05).The positive expression of group C was higher than that in group B(P<0.05).This suggested that nimodipine can promote the expression of Bcl-2.The positive expression of Bax was increased from 4W in group B and C,maintain to 8w,the comparison of three time points in the group was statistically significant(P<0.05).The positive expression of group B was higher than that in group C(P<0.05).It is suggested that nimodipine can inhibit the expression of Bax.Bcl-2/Bax all decreased in group B at 4,6,and 8w,compared with the same time point of group C was statistically significant(P<0.05),the group C had the highest ratio at 4w.This suggested that nimodipine can increase Bcl-2/Bax ratio to inhibit apoptosis.However,due to the continuous presence of high intraocular pressure,the effect at 6 and 8w is gradually decreased.4 TUNEL detection There was few apoptotic positive cells in the lateral geniculate nucleus of group A.The apoptotic positive cells of group B and C began to increase at 6 w,and then at 8w,the comparison between two time points in the group was P<0.05.The results suggested that the positive expression of apoptotic cells increased with the duration of ocular hypertension,and the positive expression of group B was higher than that in group C(P<0.05),suggested that nimodipine can inhibit the apoptosis of the lateral genicular neurons to a certain extent.Conclusions 1 Chronic ocular hypertension can reduce the number of optic axons,and cause damage to the upper lateral geniculate nerve cells.2 Nimodipine can reduce the damage of optic nerve and lateral geniculate neurons caused by chronic ocular hypertension to a certain extent,through promote the expression of anti-apoptotic factor Bcl-2 and inhibit the expression of apoptotic factor Bax. |
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