中山醫學大學機構典藏 CSMUIR:Item 310902500/24583
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    题名: Cilostazol ameliorates diabetic nephropathy by inhibiting high-glucose-induced apoptosis
    作者: Chian, CW;Lee, YS;Lee, YJ;Chen, YH;Wang, CP;Lee, WC;Lee, HJ
    关键词: Cilostazol;Diabetic nephropathy;Mesangial cell;Mitochondrial DNA;Oxidative stress
    日期: 2020
    上传时间: 2022-08-09T08:04:43Z (UTC)
    出版者: KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY
    ISSN: 1226-4512
    摘要: Diabetic nephropathy (DN) is a hyperglycemia-induced progressive development of renal insufficiency. Excessive glucose can increase mitochondrial reactive oxygen species (ROS) and induce cell damage, causing mitochondrial dysfunction. Our previous study indicated that cilostazol (CTZ) can reduce ROS levels and decelerate DN progression in streptozotocin (STZ)-induced type 1 diabetes. This study investigated the potential mechanisms of CTZ in rats with DN and in high glucose-treated mesangial cells. Male Sprague - Dawley rats were fed 5 mg/kg/day of CTZ after developing STZ-induced diabetes mellitus. Electron microscopy revealed that CTZ reduced the thickness of the glomerular basement membrane and improved mitochondrial morphology in mesangial cells of diabetic kidney. CTZ treatment reduced excessive kidney mitochondrial DNA copy numbers induced by hyperglycemia and interacted with the intrinsic pathway for regulating cell apoptosis as an antiapoptotic mechanism. In high-glucose-treated mesangial cells, CTZ reduced ROS production, altered the apoptotic status, and down-regulated transforming growth factor beta (TGF-beta) and nuclear factor kappa light chain enhancer of activated B cells (NF-kappa B). Base on the results of our previous and current studies, CTZ deceleration of hyperglycemia-induced DN is attributable to ROS reduction and thereby maintenance of the mitochondrial function and reduction in TGF-beta and NF-kappa B levels.
    URI: http://dx.doi.org/10.4196/kjpp.2020.24.5.403
    https://www.webofscience.com/wos/woscc/full-record/WOS:000562593700004
    https://ir.csmu.edu.tw:8080/handle/310902500/24583
    關聯: KOREAN JOURNAL OF PHYSIOLOGY & PHARMACOLOGY ,2020 ,v24 ,issue 5 ,p403-412
    显示于类别:[中山醫學大學研究成果] 期刊論文

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