Protective Effect Of Genistein On The Human Retinal Pigment Epithelium Cell Cultured In High Glucose

Diabetic Retinopathy, the most common microvascularcomplication of diabetes, is the first cause of blindness withspecificity change of eyeground. Some studies have indicate thatwhen hyperglycemia occurs retina may sufer oxidative damagemediated by free radical. In different cells, oxidative stress canregulate many physiological functions, biochemical reactions, andcell proliferation, diferentiation or apoptosis may occur, producingnew blood vessel. The retinal pigment epithelium (RPE) is amonolayer of pigmented cells between the endothelium of choriocapillaris and stratum neuroepitheliale retinae, forming a partof the: blood/retina barrier. It plays an important role innourishment, attendance, metabolism in retina. It suggests that highglucose can influence the growth of RPE cells and the function ofouter retina barrier.Genistein, the isoflavone of greatest interest in soy protein,has a wide variety of pharmacological effects on chemopreventionof breast and prostate cancers, prevention and treatment ofcardiovascular disease, and many other chronic diseases.Intracellularly, genistein has many different cellular mechanisms,which are shown to inhibit tyrosine kinases and DNAtopoisomerasesâ… andâ…¡, and alter the metabolism of estrogen.Resently, it has been reported that genistein is a good antioxidantpotential. It may be an effective agent in the prevention andtreatment of diabetic retinopathy.In present study, we investigateeffect of high glucose to the growth of RPE cells and the molecularevents involved in high glucose effect, focusing especially on the changes of ROS and SOD and the protective effects of genistein ofhuman RPE cells cultured in high glucose.RPE cells cultured in high glucose (33mmol/L) in vitro weretreated with genistein with different concentrations of 0,50,100,200umol/L respectively for 48h. The morphologic changes of cellswere observed by light microscopy. Cells viability were tested byMTT assay, cell cycle phase distribution of RPE cells were measuredby flow cytometry (FCM). The intracellular ROS was detected byconfocal microscopy with fluorescent probe CM-H₂DCFDA. Thevalidity of SOD was measured by Xanthine Oxidase Enzymic method.Compared to the controls, the treatment of RPE cells with33mmol/L glucose caused a obviously decrease of cellular viability,the validity of SOD, but the level of intracellular ROS was markedlyincreased.The effect of high glucose was inhibited in a positivemanner of genistein concentration.Together with our studies, we concluded that:1. High glucose can damage RPE cells. The mechanism is high glucose evoke ROS expression and disrupts the oxidativeequilibrium in RPE cells.2. High glucose disrupts the oxidative equilibrium in RPE cells,which can be inhibited by genistein.