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S. Palla, M. Saraswat, P. Y. Reddy, M. J. Petrash, G. B. Reddy; Inhibition of Aldose Reductase, Protein Glycation and Delay of Diabetic Cataract in Rats by Rutin. Invest. Ophthalmol. Vis. Sci. 2008;49(13):1467.
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© ARVO (1962-2015); The Authors (2016-present)
Activation of aldose reductase (AR)-mediated polyol pathway and increased formation of advanced glycation endproducts (AGE) have been implicated in the development of complications of diabetes including diabetic cataract. On screening, we have observed inhibition of AR and AGE formation by some commonly consumed dietary sources and rutin was found in most of these sources. In this study we investigated the potential of rutin to inhibit AR and AGE formation in vitro and tested its anticataractogenic potential in vivo using streptozotocin (STZ)-induced diabetic cataract rat model.
Inhibition of AR by rutin was assessed using rat lens and recombinant AR. Antiglycating potential of rutin was evaluated by assessing its potential to inhibit in vitro-induced glycation of lens proteins. Subsequently, rutin protective effective against diabetic cataract was investigated in STZ-induced cataract rat model.
Rutin has inhibited rat lens and human recombinant AR with IC50 15µM. Rutin at 50 µM inhibited the formation of sorbitol (50% reduction) in RBC when incubated in high glucose conditions. In addition, rutin also inhibited in vitro-induced lens protein glycation (50-80% inhibition) at 50-100-µM concentrations as assessed by SDS-PAGE, AGE-fluorescence, protein carbonyls and immunological methods. Further, when fed to diabetic rats, rutin delayed the progression and maturation of diabetic cataract in a dose dependent manner (0.02 and 0.2% in the diet) when compared to non-treated diabetic rats. Feeding of rutin delayed diabetic cataract through the inhibition of AR and protein glycation.
The results indicate that rutin is effective against development of diabetic cataract in rats.
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