Thymoquinone protects renal tubular cells against tubular injury

AbstractIn this work the effect of angiotensin II (AT II) on proximal tubular epithelial cells (pTECs) in vitro was studied. AT II was found to activate the nuclear factor κB (NF‐κB) and its controlled genes, for example, interleukin 6 (IL‐6) of pTECs in a time‐dependent manner. Two points with maximum NF‐κB activation were found, the first after 12 h and the second after 3.5 days. The first point may be due to activation of NF‐κB in pTECs in response to AT II while the second may be due to activation of the advanced glycation end product (AGE)/receptor of the AGE (RAGE) system. Thymoquinone (TQ) was found to decrease NF‐κB activation in a dose‐dependant manner with maximum inhibitory effect at a concentration of 500 nM. Also, pre‐incubation of pTECs with TQ leads to disappearance of the second peak of NF‐κB. These data are consistent with results obtained from IL‐6 enzyme‐linked immunosorbent assay (ELISA) and transient transfection experiments. The results explain the therapeutic value of TQ which can be used to delay end stage renal diseases in diabetics. Copyright © 2008 John Wiley & Sons, Ltd.