Abstract
Aim of the study:
KIOM-79 retards the development of diabetic nephropathy in animal models of type 1 and type 2 diabetes. In this study, we evaluated whether KIOM-79 could prevent apoptotic cell death and advanced glycation end products (AGEs) accumulation in the retinas of diabetic db/db mice.
Material and methods:
Mice were treated orally with KIOM-79 (150 mg/kg body weight) once daily for 12 weeks. Levels of retinal ganglion cell death were measured by terminal dUTP nick-end labeling (TUNEL) assay. In the retina, the activity of caspase-3 (a marker of apoptosis) and the formation of AGEs were measured by immunohistochemical staining.
Results:
KIOM-79 reduced the number of TUNEL-immunoreactive retinal cells. KIOM-79 attenuated caspase-3 expression and AGEs accumulation in the retina.
Conclusions:
These data show that KIOM-79 can prevent apoptosis in neuronal cells, AGEs accumulation in the retina, and retard the development of diabetic retinopathy.
Publication types
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Research Support, Non-U.S. Gov't
MeSH terms
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Administration, Oral
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Animals
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Antioxidants / pharmacology
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Antioxidants / therapeutic use*
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Apoptosis / drug effects*
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Caspase 3 / metabolism
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Cell Death / drug effects
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Diabetes Mellitus, Experimental / metabolism
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Diabetes Mellitus, Experimental / pathology
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Diabetes Mellitus, Experimental / prevention & control
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Diabetic Retinopathy / metabolism
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Diabetic Retinopathy / pathology
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Diabetic Retinopathy / prevention & control*
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Disease Models, Animal
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Glycation End Products, Advanced / antagonists & inhibitors*
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Glycation End Products, Advanced / metabolism
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Immunohistochemistry
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In Situ Nick-End Labeling
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Male
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Mice
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Mice, Inbred C57BL
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Plant Extracts / pharmacology
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Plant Extracts / therapeutic use*
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Retina / drug effects*
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Retina / metabolism
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Retina / pathology
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Retinal Ganglion Cells / metabolism
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Retinal Ganglion Cells / pathology
Substances
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Antioxidants
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Glycation End Products, Advanced
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KIOM 79
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Plant Extracts
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Casp3 protein, mouse
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Caspase 3