Cichoric acid inhibits oxidative stress in diabetes nephropathy by regulating Nrf2/HO-1
Objective To investigate the effect of cichoric acid (CA)on diabetes nephropathy (DN)and the molecular mechanism of reactive oxygen species (ROS)oxidative stress. Methods We fed C57BL/6 mice a high-fat diet and injected streptozotocin to establish a DN model. In addition,we stimulated NRK-52E cells with 20 mmol/L D-glucose to establish a DN model in vitro. C57BL/6 mice were fed with high-fat diet and injected with streptozotocin to establish DN model. NRK-52E cells were stimulated with 20 mmol/L D-glucose to establish DN model in vitro. ELISA was used to measure the levels of malondialde-hyde (MDA),superoxide dismutase (SOD),glutathione (GSH)and glutathione peroxidase (GSH-PX). Renal tissues were stained with HE,Masson and PAS,and Western blot was used to detect Nrf2 and HO-1 protein levels.Results CA reduced in-dex of kidney weight,improved glomerular structural damage,improved water intake,urine protein levels,serum creatinine,and urea nitrogen levels. In the mouse model of diabetes nephropathy,cichoric acid inhibited the level of MDA in renal tissue and in-creased the levels of SOD,GSH and GSH-PX. Meanwhile,in the in vitro model,chicory acid inhibited MDA levels in renal cells and increased SOD,GSH and GSH-PX levels. Finally,cichoric acid promoted Nrf2/HO-1 signaling pathway in kidney tis-sue of diabetes nephropathy mice and also activated Nrf2/HO-1 signaling pathway in kidney cells in vitro.Conclusion Cichoric acid reduces oxidative stress damage in DN by activating Nrf2/HO-1 signaling pathway. Cichoric acid may be a promising thera-peutic drug for treating or preventing diabetes nephropathy.
万方数据
维普
