title: Thymoquinone protects renal tubular cells against tubular injury.
abstract: In 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 kappaB (NF-kappaB) and its controlled genes, for example, interleukin 6 (IL-6) of pTECs in a time-dependent manner. Two points with maximum NF-kappaB 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-kappaB 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-kappaB 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-kappaB. 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.
authors.affiliation: Chemistry Department, Faculty of Science, Minia University, El-Minia, Egypt. sayedaar@yahoo.de
authors.forename: Ahmed Amir Radwan
authors.initials: AA
authors.lastname: Sayed
mesh_terms: D000328:Adult; D016227:Benzoquinones / Q000494:pharmacology*; D002478:Cells, Cultured; D019610:Cytoprotection / Q000187:drug effects*; D006801:Humans; D007674:Kidney Diseases / Q000473:pathology*; D007687:Kidney Tubules, Proximal / Q000187:drug effects* / Q000473:pathology*; D016328:NF-kappa B / Q000378:metabolism; D010957:Plasmids / Q000235:genetics; D011485:Protein Binding / Q000187:drug effects; D014158:Transcription, Genetic / Q000187:drug effects; D015533:Transcriptional Activation / Q000187:drug effects; D014162:Transfection
chemical_list: D016227:Benzoquinones; D016328:NF-kappa B; C003466:thymoquinone