title: Quercetin suppresses NF-κB and MCP-1 expression in a high glucose-induced             human mesangial cell proliferation model.
abstract: Diabetic nephropathy (DN), which is characterized by mesangial cell proliferation, is a common complication observed in diabetic patients. The protective effects of quercetin for DN have been reported; however, the mechanism has yet to be determined. We aimed to identify the underlying mechanism for quercetin protection against DN. High glucose (HG)-induced human mesangial cell (HMC) proliferation, a feature of the early stages of diabetic nephropathy, was employed as an in vitro model. Cells were grown in normal glucose (5.6 mM), high glucose (30 mM) or high glucose with various concentrations of quercetin. Cell proliferation, cell cycle progression, and expression of NF-κB and MCP-1 were examined by MTT assay, DNA staining, immunocytochemistry and western blot analysis, respectively. HMCs cultured in high glucose had signficantly greater proliferation, accumulation in the G1 phase, upregulated NF-κB and MCP-1 expression. Quercetin treatment reversed the effects of high glucose in a dose-dependent manner. Cotreatment of quercetin with pyrrolidine dithiocarbamate (PDTC), an inhibitor of NF-κB activation, suggest that the effects of quercetin are partially mediated by NF-κB signaling. Quercetin partially suppresses the effects of high glucose in HMC cultures, which are mediated at least in part through the suppression of NF-κB.
authors.affiliation: Fuzhou General Hospital of Nanjing Military Command, Fuzhou,                     Fujian 350025, P.R. China.
authors.forename: Pin
authors.initials: P
authors.lastname: Chen
authors.forename: Qiyang
authors.initials: Q
authors.lastname: Shi
authors.forename: Xiangjin
authors.initials: X
authors.lastname: Xu
authors.forename: Yanqiao
authors.initials: Y
authors.lastname: Wang
authors.forename: Wenyu
authors.initials: W
authors.lastname: Chen
authors.forename: Huiling
authors.initials: H
authors.lastname: Wang
mesh_terms: D059447:Cell Cycle Checkpoints / Q000187:drug effects; D002460:Cell Line; D049109:Cell Proliferation / Q000187:drug effects; D018932:Chemokine CCL2 / Q000096:biosynthesis / Q000378:metabolism*; D003920:Diabetes Mellitus / Q000473:pathology; D003928:Diabetic Nephropathies / Q000188:drug therapy / Q000473:pathology; D005947:Glucose / Q000494:pharmacology*; D006801:Humans; D007249:Inflammation; D007668:Kidney / Q000187:drug effects / Q000378:metabolism; D050527:Mesangial Cells / Q000166:cytology / Q000187:drug effects / Q000378:metabolism*; D016328:NF-kappa B / Q000037:antagonists & inhibitors / Q000096:biosynthesis / Q000378:metabolism*; D011759:Pyrrolidines / Q000494:pharmacology; D011794:Quercetin / Q000494:pharmacology*; D015398:Signal Transduction / Q000187:drug effects; D013859:Thiocarbamates / Q000494:pharmacology; D051996:Transcription Factor RelA / Q000096:biosynthesis / Q000378:metabolism
chemical_list: C111835:CCL2 protein, human; D018932:Chemokine CCL2; D016328:NF-kappa B; D011759:Pyrrolidines; D013859:Thiocarbamates; D051996:Transcription Factor RelA; C020972:pyrrolidine dithiocarbamic acid; D011794:Quercetin; D005947:Glucose