期刊
EXPERIMENTAL CELL RESEARCH
卷 319, 期 20, 页码 3182-3189出版社
ELSEVIER INC
DOI: 10.1016/j.yexcr.2013.10.006
关键词
Emodin; Mesangial cells; High glucose; NF-kappa B; TGF-beta 1; FN
资金
- Natural Science Foundation of China [81200308, 81201622, 81260324]
- Natural Science Foundation of Guangdong Province, China [S2012040008026]
- Project of Guangdong University of outstanding young talents cultivation [2012LYM_0081]
- Zhujiang Technology New Star of Guangzhou City [2013J2200025]
The activation of nuclear factor-kappa B (NF-kappa B) and the subsequent overexpression of its downstream targets transforming growth factor-beta 1 (TGF-beta 1) and fibronectin (FN) are among the hallmarks for the progressive diabetic nephropathy. Our previous studies demonstrated that emodin ameliorated renal injury and inhibited extracellular matrix accumulation in kidney and mesangial cells under diabetic condition. However, the molecular mechanism has not been fully elucidated. Here, we showed that emodin significantly attenuated high glucose-induced NF-kappa B nuclear translocation in mesangial cells. Interestingly, emodin also inhibited the DNA-binding activity and transcriptional activity of NF-kappa B. Furthermore, NF-kappa B-mediated TGF-beta 1 and FN expression was significantly decreased by emodin. These results demonstrated that emodin suppressed TGF-beta 1 and FN overexpression through inhibition of NF-kappa B activation, suggesting that emodin-mediated inhibition of the NF-kappa B pathway could protect against diabetic nephropathy. (C) 2013 Elsevier Inc. All rights reserved.
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