Protective Effect of Bushen Yiqi Huoxue Fang on Retinal Oxidative Damage in Model Mice of Dry Age-Related Macular Degeneration

OBJECTIVE The study was aimed at evaluating protective effect of Bushen Yiqi Huoxue Fang on retinal oxidative damage in model mice of dry age-related macular degeneration (AMD) and to elucidate the underlying mechanism. METHODS 60 six-month-old C57BL/6 female mice， 10 were fed normal diet as aging control， 50 were fed a high-fat diet for 6 months followed by HQ (0.8%) in the drinking water for 3 months to established dry AMD model mice . Model mice were divided randomly into vehical control， positive drug(lutein) and 3 treatment groups (dosage:low，middle，high) .Drugs were given once-daily through gastrogavage for 3 months. At the end of the experimental period， the mice were killed and the eyes immediately removed. Transmission electron microscopy were used to evaluate sub-RPE deposit formation and Bruch membrane (BrM ) thickness; The serum were separated from the blood sampling of mice eye vein， mice retina were detached and homogenated， the serum and retina SOD， GSH-PX， CAT enzyme activity and ROS， MDA content were detected; The mRNA and protein expression of Nrf2， HO-1， NQO-1， GCL were detected by qPCR and Western blot， respectively. RESULTS Compared with aging control mice， the sub-RPE deposits was significantly increased， and the Bruch membrane was significantly thickened in vehical control mice; Bushen Yiqi Huoxue Fang can significantly inhibit sub-RPE deposit formation and reduce thickening of BrM in model mice compared to the vehical control mice， the sub-RPE deposits was decreased， BrM thickness was inhibited in treatment mice. Bushen Yiqi Huoxue Fang could increase SOD， GSH-PX and CAT enzyme activity， reduce ROS， MDA content of retina and serum in mice. mRNA and protein expressions of Nrf2， HO-1，NQO-1， GCL of HO-1， NQO-1 were up-regulated in mice treated with Bushen Yiqi Huoxue Fang(middle， high dosage) . CONCLUSION Bushen Yiqi Huoxue Fang could protect the retina against oxidative damage in model mice of dry AMD， the underlying mechanism may be to increase SOD， GSH-PX and CAT enzyme activity and up-regulate expressions of Nrf2， HO-1，NQO-1， GCL through activation of Nrf2 pathway， which may strengthen the clearance of reactive oxygen species in model mice.