Genistein attenuates parathyroid hormone-induced renal interstitial fibrosis through inhibiting NF-κB signaling pathway
10.3760/cma.j.issn.1001-7097.2010.12.005
- VernacularTitle:金雀异黄素通过抑制NF-κB信号通路延缓甲状旁腺素诱导的肾间质纤维化
- Author:
Yunshan GUO
;
Weijie YUAN
;
Aiping ZHANG
;
Yaohai DING
;
Yanxia WANG
- Publication Type:Journal Article
- Keywords:
Parathyroid hormone;
Fibrosis;
Epithelial cells;
Kidney tubules;
Genistein;
Connective tissue growth factor;
Signaling pathway
- From:
Chinese Journal of Nephrology
2010;26(12):898-903
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the role of genistein (Gen) in the expression of connective tissue growth factor (CTGF) induced by parathyroid hormone (PTH) in human renal tubular epithelia cells. Methods Real-time PCR, Western blotting and reporter gene assay were employed to detect the role of Gen in PTH-induced CTGF expression in HK-2 cells. The activity of NF-κB was measured by EMSA to investigate the mechanism by which PTH induced CTGF expression in HK-2 cells. Inhibitors of NF-κB signaling pathway were used to ascertain which signal pathway was involved. Results HK-2 cells had basic amount of CTGF mRNA and protein, which, however, increased significantly after treatment with PTH, and the luciferase activity increased to a higher level as compared with control group after treatment with 10-10 mol/L PTH for 12 h (1.89±0.08 vs 0.99±0.03, P＜0.01). Gen decreased the expressions of CTGF mRNA and protein induced by PTH in dose-dependent manner. The NF-κB of nucleus was inactivation without PTH, while the activity of NF-κB significantly increased after exposed to PTH, with the maximal response of PTH at a concentration of 10-10 mol/L and the best stimulating time at 30 minute. The NF-κB inhibitor PDTC reduced the increase of CTGF transcript levels in response to PTH stimulation. Gen blunted PTH-mediated NF-κB activation. Conclusion Gen inhibits CTGF expression induced by PTH through bloking NF-κB signaling pathway in human renal tubular epithelial cells.
