Experimental Study Of The Mechanism Of Retinal Ultraviolet Light Damage In Kunming Mice

Objectives 1. To manufacture ideal retinal ultra-violet light damage model in kunming mice .2.To approach the effect of the Fas,FasL,Bcl-2,Bax protein in the occurrence and development of retinal ultraviolet light damage.Methods 30 Kunming mice were randomly divides into the normal control group and experimental group. The experimental group were divided into the ultraviolet ray illumination 1, 2, 3, 4 weeks groups respectively . All mice were raised in cyclic light envioronment for 7 days and then kept in darkness for 36 hours before experiment. The experimental group were exposed to 2200±138Lux illuminations of ultra-violet rays for continuous 8 hours every day to establish the model of retinal ultra-violet light damage.The eye were enucleated after exposured 1, 2, 3, 4 weeks separately, the right were make HE and Fas, FasL, Bcl-2, Bax dye, simultaneously the left eye were examined the SOD vigor and the MDA content change of the retinal refining ; to observe the morphology of the retinal change for the light microscope and to analyze the differentce of the thickness of the outer nucleus layer (ONL) in each group,useing the immunity histochemistry dyeing compares to the expression quantity difference.of Fas, FasL, Bcl-2 and Bax in each group .Results 1. In front of the illumination, the normal mouse's retinal layer is clear, the organizational structure is clear.The inner and outer segment were neat and orderly arrangement,and the outer nucleus layer (ONL)arranged concinnous, the dyeing is even, the cellular form is neat,the dyeing of Fas, FasL, Bcl-2, Bax is negative or weak. After illumination, the mouse retinial photoreceptor cellular layer appeared the light damage, the light microscope show the outside segment is vacuolar degeneration in varying degree, the inside and outside segment is arranged disorder, swelling, obtrite . The outer nuclear layer changed thin, sparser and disorderly ,the injury is deteriorated gradually along with the progression of light exposure. The Fas,FasL protein start to see the positive cell or express augmented after 1 week exposure respectively, and along with the time, the expression is strengthen, when 3w reaches the peak;The Bcl-2 protein was enhanced slightly along with the illumination time ; The Bax expression was strengthened continually. 2.Analyzing the thickness of the outer nucleus layer (ONL) in each group via Photo Analysis System, we found that significant difference of the thickness changes in the outer nucleus layer between the control group and the experimental group(P<0.05),ONL was reduced in the experimental group,and there is a significant difference between the experimental groups except 3w and 4w(P<0.05). 3. There is a significant difference of the SOD vigor and the MDA content between the control group and the experimental group (P<0.05) .Conclusion The ultra-violet A and B rays can cause the mouse retinal light damage; Its extent of damage depends on the strength of illumination and time. Lipin peroxidation and free radical production have a relationship with the retinal ultra-violet light damage. Apoptosis related gene protein Fas, FasL hasten the development of the retinal ultra-violet light damage,and Bax is also speeded up the damage. Apoptosis repressed gene protein Bcl-2 can't inhibit the cell apoptosis.