Baicalein reduces inflammatory process in a rodent model of diabetic retinopathy

PURPOSE. This study was designed to elucidate the role of inflammatory process in diabetic retinopathy and to investigate the effect of baicalein treatment on diabetic rat. METHODS. Retinal microglial cells were identified with CD11b antibody, and retinal Müller cells were identified with glial fibrillary acidic protein (GFAP). The gene expression of inter-leukin (IL)-18, tumor necrosis factor (TNF)-α, and IL-1β was examined by quantitative real-time PCR. The expression of GFAP and vascular endothelial growth factor (VEGF) was ex-amined by quantitative real-time PCR, immunohistochemistry, and Western blot analysis. Vascular permeability was measured in vivo by bovine serum albumin conjugated with FITC. Baica-lein was given by oral administration (150 mg/kg/d) with an animal feeding needle beginning 5 days after streptozotocin (STZ) injection. RESULTS. By 24 weeks after onset of diabetes, microglial cells were activated and proliferated, and Müller cells upregulated their GFAP and VEGF expression. Pro-inflammatory factors, including IL-18, TNF-α, and IL-1β, were significantly upregulated. Obvious vascular leakage and abnormality were demon-strated, and ganglion cell loss was significant. Baicalein treat-ment ameliorated diabetes-induced microglial activation and pro-inflammatory expression, reduced the GFAP and VEGF expression from Müller cells, and significantly reduced vascu-lar abnormality and ganglion cell loss within the retina. CONCLUSIONS. Inflammatory process, characterized by micro-glial activation and Müller cells dysfunction, was implicated in STZ-induced diabetic retinopathy. Baicalein treatment amelio-rated inflammatory process, and therefore inhibited vascular abnormality and neuron loss in diabetic retinas.