Baicalein reduces inflammatory process in a rodent model of diabetic retinopathy.
OBJECTIVE
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 interleukin (IL)-18, tumor necrosis factor (TNF)-alpha, and IL-1beta was examined by quantitative real-time PCR. The expression of GFAP and vascular endothelial growth factor (VEGF) was examined by quantitative real-time PCR, immunohistochemistry, and Western blot analysis. Vascular permeability was measured in vivo by bovine serum albumin conjugated with FITC. Baicalein 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-alpha, and IL-1beta, were significantly upregulated. Obvious vascular leakage and abnormality were demonstrated, and ganglion cell loss was significant. Baicalein treatment ameliorated diabetes-induced microglial activation and pro-inflammatory expression, reduced the GFAP and VEGF expression from Müller cells, and significantly reduced vascular abnormality and ganglion cell loss within the retina.


CONCLUSIONS
Inflammatory process, characterized by microglial activation and Müller cells dysfunction, was implicated in STZ-induced diabetic retinopathy. Baicalein treatment ameliorated inflammatory process, and therefore inhibited vascular abnormality and neuron loss in diabetic retinas.
Yang
Li-ping
LP
Peking University Eye Center, Peking University Third Hospital, Peking University, Beijing, PR China.
Sun
Hui-li
HL
Wu
Le-meng
LM
Guo
Xiu-juan
XJ
Dou
Hong-liang
HL
Tso
Mark O M
MO
Zhao
Lin
L
Li
Shun-min
SM
D000284:Administration, Oral; D000818:Animals; D000893:Anti-Inflammatory Agents / Q000627:therapeutic use*; D001786:Blood Glucose / Q000032:analysis; D001813:Blood-Retinal Barrier / Q000187:drug effects; D015153:Blotting, Western; D039481:CD11b Antigen / Q000378:metabolism; D002199:Capillary Permeability / Q000187:drug effects; D003921:Diabetes Mellitus, Experimental / Q000188:drug therapy*; D003930:Diabetic Retinopathy / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D005260:Female; D044950:Flavanones / Q000627:therapeutic use*; D019084:Fluorescent Antibody Technique, Indirect; D005904:Glial Fibrillary Acidic Protein / Q000378:metabolism; D020382:Interleukin-18 / Q000235:genetics; D053583:Interleukin-1beta / Q000235:genetics; D017628:Microglia / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D012333:RNA, Messenger / Q000378:metabolism; D051381:Rats; D017207:Rats, Sprague-Dawley; D055351:Retinal Neurons / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology; D012173:Retinitis / Q000188:drug therapy* / Q000378:metabolism / Q000473:pathology; D020133:Reverse Transcriptase Polymerase Chain Reaction; D014409:Tumor Necrosis Factor-alpha / Q000235:genetics; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism
D000893:Anti-Inflammatory Agents; D001786:Blood Glucose; D039481:CD11b Antigen; D044950:Flavanones; D005904:Glial Fibrillary Acidic Protein; D020382:Interleukin-18; D053583:Interleukin-1beta; D012333:RNA, Messenger; D014409:Tumor Necrosis Factor-alpha; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; C006680:baicalein