KMID : 1235920090010020215
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Medical Journal of Catholoc University of Daegu 2009 Volume.1 No. 2 p.215 ~ p.220
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Suppressive Effect of Estrogen on the Mesangial Hypertrophy of Rat Kidney Induced by Advanced Glycation End Products
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Cho Chang-Ho
Oh Hoon-Kyu Kum Yoon-Seup Park Kwan-Kyu Lee In-Hee Ahn Ki-Sung Park Jae-Bok
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Abstract
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Purpose: Advanced glycation end products (AGEs), have been implicated in the pathogenesis of diabetic glomerulosclerosis. Although estrogen is known to be renoprotective, the mechanism has not been fully elucidated.
Therefore, the aim of this study is to investigate the effect of estrogen on the mesangial hypertrophy induced by AGEs.
Material and Methods: We prepared distinct AGEs from incubation of bovine serum albumin. The mesangial cells
were isolated from rat kidneys and cultured with AGEs or AGEs with estradiol. The activity of mesangial cells were measured by MTT assay. The apoptosis rate and cell cycle-associated Ki-67 protein expression level were examined
by immunocytochemical stain and counted under microscope.
Results: AGEs increased activity of mesangial cells in a dose-dependent manner at the level lower than 200 ug/mL. By the adding of estradiol, the cellular activity was decreased. The AGEs suppressed the apoptotic rate. When
estradiol was supplemented, the apoptotic rate was increased again. Ki-67 protein expression, a kind of cell proliferative index, was not changed in the mesangial cells administered with AGEs only or administered with AGEs plus estradiol.
Conclusion: AGEs induced increase of the cell activity and decrease of the apoptotic rate, which will result in
mesangial hypetrophy of glomeruli. The estradiol reverses the cellular activity and apoptotic rate of mesangial cells induced by AGEs. Estrogen is thought to be a useful drug for the treatment of diabetic glomerulopathy.
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KEYWORD
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Advanced glycation end products, Estrogen, Mesangial cells, Apoptosis
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