Protective Effects of Kaempferitrin on Advanced Glycation End Products Induce Mesangial Cell Apoptosis and Oxidative Stress

被引:46
作者
Jiang, Wenxian [1 ]
Wang, Rongshen [1 ]
Liu, Di [1 ]
Zuo, Min [1 ]
Zhao, Chunzhen [1 ]
Zhang, Tianliang [2 ]
Li, Wanzhong [1 ]
机构
[1] Weifang Med Univ, Sch Pharm, Weifang 261053, Peoples R China
[2] Weifang Med Univ, Expt Ctr Med Res, Weifang 261053, Peoples R China
关键词
kaempferitrin; mesangial cells; advanced glycation end products; oxidative stress; apoptosis; signal pathway; DIABETIC KIDNEY-DISEASE; CYTOCHROME-C RELEASE; GLUCOSE-UPTAKE; RECEPTOR; AGES; PATHWAY; NEPHROPATHY; ACTIVATION; MECHANISMS; PROTEINS;
D O I
10.3390/ijms19113334
中图分类号
Q5 [生物化学]; Q7 [分子生物学];
学科分类号
071010 ; 081704 ;
摘要
Advanced glycation end products (AGEs) and the receptor for AGEs (RAGE) both play important roles in diabetic nephropathy (DN). Previous studies have identified glomerular mesangial cells (GMCs) injury as a key early risk factor in the development of DN. Kaempferitrin (KM) is a potent antioxidant with hypoglycemic action. Although KM is known to protect against AGE-induced damage in GMCs, the effects and the mechanisms by which they occur are poorly understood. In this study, cultured rat GMCs were exposed to AGE-induced oxidative stress (OS) to model DN in vitro. Reactive oxygen species (ROS) was analyzed by 2',7'-dichlorofluorescin diacetate (DCFH-DA). Superoxide dismutase (SOD) and malondialdehyde (MDA) were studied using commercial kits. Mitochondrial membrane potential (m) was measured by rhodamine 123. Hoechst 33258 and annexin V and propidium iodide (PI) double staining were performed to observe the apoptosis states in GMCs, whereas apoptosis and protective mechanism in AGE-induced GMCs were investigated by Western blot. The data revealed that KM effectively increased SOD activity, decreased MDA levels, suppressed ROS generation, and protected against OS in AGE-induced GMCs. Treatment with KM also inhibited the expression of collagen IV and transforming growth factor-beta 1 (TGF-beta 1), improved mitochondrial membrane potential recovery, and suppressed the mitochondrial/cytochrome c-mediated apoptosis pathway through the expression of anti-apoptotic factors in GMCs in vitro. These findings suggest that KM may be a new potential agent in the treatment of DN in future.
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页数:13
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