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Masami Nakajima, Michael J. Cooney, Alexander H. Tu, Kwang Yul Chang, Jingtai Cao, Akira Ando, Gi-Jung An, Michele Melia, Eugene de Juan; Normalization of Retinal Vascular Permeability in Experimental Diabetes with Genistein. Invest. Ophthalmol. Vis. Sci. 2001;42(9):2110-2114.
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purpose. To study the effects of genistein, a tyrosine kinase inhibitor, on
retinal vascular permeability in an experimental diabetic rat model.
methods. Seventy-two rats were equally divided into four groups: (1) nondiabetic
control group, (2) diabetic control group, (3) diabetic rats receiving
150 mg genistein/kg food, and (4) diabetic rats receiving 300 mg
genistein/kg food. Diabetes was induced by streptozotocin injection in
the three diabetic groups. Rats were fed diets with or without
genistein and followed for 6 months. Retinal vascular permeability was
assessed by measuring radiolabeled sucrose leakage into the retina and
by Western blot analysis for total retinal albumin. Retinal
phosphotyrosine levels and proliferating cell nuclear antigen (PCNA)
were also evaluated by Western blot analysis.
results. Diabetic control rats had markedly increased retinal vascular leakage
of radiolabeled sucrose compared with nondiabetic control rats.
Diabetic rats receiving oral genistein had significantly less retinal
vascular leakage of radiolabeled sucrose than diabetic control rats in
a dose–response fashion. Diabetic control rats had increased levels of
phosphotyrosine, retinal albumin, and PCNA by Western blot analysis
compared with nondiabetic control rats. Rats receiving 300 mg of
genistein had decreased retinal albumin by Western blot analysis.
Western blot analysis demonstrated a dose–response decrease in retinal
phosphotyrosine levels and PCNA in genistein-treated diabetic rats
compared with diabetic control rats.
conclusions. Long-term oral administration of genistein significantly inhibits
retinal vascular leakage in experimentally induced diabetic rats.
Tyrosine kinase inhibition may be a useful pharmacological approach for
the treatment of diabetic-induced retinal vascular
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