A Correlative Study Of Homocysetineand Human Trabecular Meshwork Function Of Primary Open-angle Glaucoma

Objective: To research the homocysteine(Hcy) on the human trabecular meshwork of oxidative stress status and influence of functional dysfunction. To probe pathogenesis of Hcy mediated oxidative stress reaction in the role of primary open-angle glaucoma(POAG) in order to provide experimental basis for the early diagnosis of POAG.Methods:(1)This study collected patients with POAG and senile cataract patients.The Hcy concentration of plasma and aqueous humor were measured using enzymatic cycling assay.(2)Human trabecular meshwork cells( HTMCs) were cultured after 4 to 6 generations were randomly divided into 5 groups.Blank control group:the normal cultured HTMCs, the experimental group: normal cultured HTMCs + Hcy( Hcy concentration respectively 30 μmol/L, 100μmol/L, 300μmol/L, 1000μmol/L).Trabecular meshwork cells proliferation with CCK-8, mitochondrial membrane potential levels were detected with JC-1, flow cytometry to detect the release of ROS.Using western blot analysis,the expression of SOD1 was detected.Results:(1) The POAG group of Hcy concentration in plasma, aqueous humor(14.44±0.86 、 1.603±0.27μmol/L) were higher than in senile cataract group(10.82±0.29、0.686±0.39μmol/L), P < 0.01, the difference is statistically significant;(2) Compared with the blank control group, the cell apoptosis rate of different concentration Hcy in each HTMCs group with statistical difference(P < 0.001);(3) With increasing of concentrations between Hcy group,mitochondrial membrane potential of Hcy concentration, increased formation of ROS, SOD1 expression reduce, the concentration difference between groups had significant difference(P < 0.01),Conclusion: This research suggests POAG patients with elevated Hcy concentration in both plasma and aqueous humor, may be the risk factor of POAG;Hcy can promote apoptosis of HTMCs,induce the oxidative stress of human trabecular meshwork cells, the incidence of POAG have certain relevance.