BU JINGYISHI Tablet Control Research On MNU-induced Photoreceptor Apoptosis Signaling Pathway

Objective:This article is to study the n-methyl-n-nitrosourea which induced retinal photoreceptor apoptosis of the rat retina photosensitivity cell model, discuss the Bu JingYiShi tablet on the regulatory mechanism of signal process of photoreceptor cell apoptosis and acting targets and molecular mechanism of the treatment retinal degenerative diseases, take retinitis pigmentosa which with photoreceptor cell apoptosis as the common pathological features for the representative eye, aimed from different angles to explore the effect and mechanism of Bu JingYiShi tablet in the treatment of the same type of eye disease, Provide a guidance for clinical, also provide new ideas and methods of Chinese herbs in the future prevention and treatment of retinal degeneration diseases.Methods:Establish MNU SD induced rat retinal photosensitive cells apoptosis model, using mfERG histopathological technology (optical, electron microscopy), TUNEL method, observing Bu JingYiShi tablet model in Rat Retina after the intervention function, morphology, changes of ultrastructure and apoptosis of photoreceptor cell, use proteins Immunohistochemistry and immunoblotting (Western Blot) to exploreBu JingYiShi tablet on MNU-induced photoreceptor cells in the rats retina activity before apoptosis signal transduction factor of P53, Cyt-C, Apaf-1, Caspase-9protein expression changesResults:①After modeled24h, the amplitude of N1and P1wave of mfERG decreased and peak latencies extended in the model group. By light and electron microscopy, it showed that the outer nuclear layer was thinning, the structural was disorder, the nuclear pyknosis, structural of outer section plate membrane in photoreceptor were abnormal. Photoreceptor apoptosis rate was significantly increased by Tunel method, it suggested that the model was successful, the difference was statistically significant(P<0.05). And dose-filter study showed that MNU40mg was the best dose, the difference was statistically significance (P<0.05).②After modeled10days and14days, mfERG test in each group showed that the amplitude and peak latencies of N1and P1wave all recovered after given Vitamin A and Bu JingYiShi tablets, and morphological observation suggests that there was better repairing damaged tissue and protecting photoreceptor cells continue to apoptosis in vitamin A group and Bu JingYiShi tablet group. Bu JingYiShi tablet group was better than Vitamin A group, the difference was statistically significance [P<0.05).③After modeled10days and14days, protein expression changes of P53,Cyt-C and protein expression of Apaf-1, Caspase-9in each group all raised, the difference was statistically significant [P<0.05). It suggested that P53, Cyt-C, Apaf-1and Caspase-9can control photoreceptor cells apoptosis. Compared treatment group with negative control group, the protein expression were different degrees of dropping, the difference was statistically significant (P<0.05), Bu JingYiShi tablet group was better than Vitamin A group (P<0.05). It pointed that JingYiShi tablet could inhibit photoreceptor cells apoptosis through lowering the protein expression of signal transduction active factors before the photoreceptor cells apoptosis.Conclusion:Bu JingYiShi tablets could inhibit photoreceptor cel Is apoptosis through lowering the protein expression of signal tran sduction active factors P53, Cyt-C, Apaf-1, Caspase-9before the ph otoreceptor cells apoptosis. Thus it could play a role of protecting retinal function, reducing damage of photoreceptors and preventin g retinal degeneration.