The Study Of Activation Glaucoma Retinal Ganglion Cells Protection Pathway Based On The Liver

Objective:To investigate the clinical through self orifices TongqiaoMingmu No.4on glaucomatous optic neuropathy protective effects and molecular mechanism, Provide direct evi-dence for traditional Chinese medicine prescription to protect neurons.Materials and methods:Intraperitoneal injection of10%chloral hydrate anesthesia in mice (3.8ml/kg), And with Aobukayinkayin hydrochloride eye drops in local anesthesia,and dilated with mydrinp eye drops.Using unilateral anterior chamber injection method of the compound carbomer solution on adult SD rats to establish chronic high intraocular pressure model. After the success of modeling, The high IOP after one week in rats, Gave orifices Tong qiaoMingmu No.4in low dose, middle dose, high dose were treated for two weeks, and use vitamin B1, B12as the control group of Western medicinetherapy. Signal transduction and transcription in the retina of rats with chronic intraocular hyper-tension in activating factor3(STAT3)、RGCs、 Bcl-xl for interventions targeting, the histopathological observation、 immuno-histochemical、Western blot and cell ultrastructure of detection method, from the whole and cells、genes levels systematically orifices Tongqiao Mingmu No.4on glaucoma optic effect and molecular mechanism of neural protection,quantitative analysis of optic nerve protective effe-ct about the orifices Tongqiao Mingmu No.4Between the two groups using indep-endent sample T test,it used single factor analysis of variance comparison between groups, p<0.05is considered to have differences, statistically significant, p<0.01was significant difference.Result:1.The blank group retinal ten layerstructure is clear under light microscope,retinal ganglion cells were clearly visible, no edema. The retina became thinning at first and became thick after high intraocular pressure, the interlayer structure is not clear, arranged disorder, increased vesicular structure, the number of ganglion cells reduced, inflammatory cell infiltration. retinal damage was obviously lighter than the model group after Tong Qiao ming mu No4treatment, the retinal structure of each layer was somewhat disorder, the ganglion cell arranged loosely, visible vacuole, cell number increased in comparison with the model group, to reduce the degreeof retinaledema.2.The structure of glial cells and thenerve ganglion cells was normal in the blank group under the Electron microscopic, the cells mitochondria was rich, Outer segment structure is normal, the membrane discarranged closely. Structure set of ganglion cells high intraocular pressurefuzzy, organelle disappear, mitochondria swelling, cytoplasmvacuolar degeneration, synaptic integration, lap dissolve. After drug treatment and vacuolar degeneration compared with model control group, reduce the number of ganglion cells, clear membrane, endoplasmic reticulum, mitochondria structure basically normal cytoplasm. After treatment of mitochondria edema, the synapticstructure is relatively clear, reduce the degree of disc membrane fusion.3.Immunohistochemistry and Western blot indicated:blank group of retinal STAT3, Bcl-xl rats showed low expression, high intraocular pressure model showing expression of mild upward trend, after drug treatment, the expression increased significantly,show tong qiao ming mu No4activation of the optic pathway protection channel.Conclusion:Tong qiao ming mu No4on glaucomatous optic nerve, retina damage,repair the exact, improve the RGCs microenvironment, the protection of intact cells,delay or prevent part damage celldegeneration. The changes of retinal pathological.It can reduceand delay caused by high intraocular pressure, deformation correcting reversible cell. It can reduce the apoptosis of high intraocular pressure RGCs. It can activate STAT3pathway upregulation of the antiapoptotic gene, plays a neuroprotective role of this pathway, including induction and regulation of immune responses, through the integration of DNA repair, mitochondrial repair, a variety of ways to play the role, sothe early application of STAT3agonists can delay or avoidacute light damage or mutation neuron s tune induction of apoptosis.Therefore it can effectively protect the retina,optic nerve, activation of the STAT3 pathway,and upregulation of the antiapoptotic gene, effectively protect the optic nerve and retina.