CPDT Affects Expression Of Bcl-2 And Bax Under High Glucose Effect In Rat Müller Cells

Diabetic retinopathy(diabetic retinopathy DR) will change cell metabolism and insulin hormone, eye, nerve and blood vessel of microcirculation, finally causes the damage of the nutrition and the visual function of the eye. The composition change of diabetes blood, will cause the abnormal function of vascular endothelium cell, and also make the blood-damaged retina barrier, bleeding spots, rigid seepage and capillary pathological changes of macular edema and so on performance, widely ischemia may cause the retina or optic disk new blood vessels, retinal hemorrhage and tractional retinal detachment So the diabetic retinopathy is one of the main factors that will cause blindness. Müller cells is one of the largest retinal glial cells in the retina and the optic nerve cells have the function of the protection and support.High glucose is very important to diabetic retinopathy, also is key factors ofthe damage in diabetic retinopathy. The Bcl- 2 family protein is the main channel of cell apoptosis. Including the Bcl- 2 in the mitochondrial membrane outside the role of antiapoptotic is the monitor of maintain the stability and the integrity of the mitochondrial membrane. The CPDT for optic nerve cells plays a protective role. To study the effects of CPDT on Bcl-2 and Bax protein expressions and apoptosis in rat müller cells under high glucose.Methods: we use under inverted phase contrast microscope to observe the cell damage under high sugar,which will make a SD rats müller cells damage model. Use primary culture SD rat müller cells which randomly divided into 3 groups :normal control group, high glucose group, CPDT control group. We use FITC/PI Current test to identify the apoptosis and cell cycle of cells. The method of Western blotting were used to measure the expression of Bcl-2 and Bax at protein levels. Result: Compared to normal control group, the FITC/PI Current test show that the apoptosis rate of high glucose group were higher. However compared with high glucose group the CPDT control group could decrease the rate of apoptosis. Each cell cycle no obvious change.Compared to normal control group, the protein expression of Bax increased obviously and the ratio of Bcl-2/Bax decreased in high glucose group.Compared to high glucose group, the protein expression of Bcl-2 and Bax decrease in CPDT control group. Conclusion:High glucose could reduce the activity of rat müller cells and make contribution to cell apoptosis. The Bcl-2under high sugar showed the protection of cells. CPDT could restore cell activity, and increase the expression of Bcl-2 and the rate of Bcl-2/Bax, inhibit the expression of Bax protein.CPDT on Bcl- 2 protein a key protein protection,prevent subsequent complex such as cytochrome C combined with casepase9 into apoptosis, speculated that CPDT may have a role in diabetic retinopathy.