[1] Pelletier J P, Martel-Pelletier J, Abramson S B. Osteorthritis, an inflammatory disease: Potentialimplication for the selection of new therapeutic targets[J]. Arthritis & Rheumatism, 2001, 44(6): 1237-1247.[2] Hida T, Yatabe Y, Achiwa H, et al. Increased expression of cyclooxygenase 2 occurs frequently in humanlung cancers, specifically in adenocarcinomas [J].Cancer Research, 1998, 58(17): 3761-3764.[3] Spielman L, Winger D, Ho L, et al. Induction of the complement component C1qB in brain of transgenicmice with neuronal overexpression of human cyclooxygenase-2 [J]. Acta Neuropathol, 2002, 103(2): 157-162.[4] Lu Y, Zhao W Z, Chang Z, et al. Procyanidins from grape seeds protect against phorbol ester-induced oxidativecellular and genotoxic damage [J]. Acta Pharmacologica Sinica, 2004, 25(8): 1083-1089.[5] Sharma S D, Meeran S M, Katiyar S K. Proanthocyanidins inhibit in vitro and in vivo growth of humannon-small cell lung cancer cells by inhibiting the prostaglandin E2 and prostaglandin E2 receptors [J].Molecular Cancer Therapeutics, 2010, 9(3): 569-580.[6] Yang F, Bleich D. Transcriptional regulation of cyclooxygenase-2 gene in pancreatic β-cells [J]. Journalof Biological Chemistry, 2004, 279(34): 403-411.[7] Saunders M A, Sansores-Garcia L, Gilroy D W, et al. Selective suppression of CCAAT/enhancerbindingprotein β binding and cyclooxygenase-2 promoter activity by sodium salicylate in quiescent humanfibroblasts [J]. Journal of Biological Chemistry, 2001, 276(22): 897-904.[8] Shaik M S, Chatterjee A, Singh M. Effect of a selective cyclooxygenase-2 inhibitor, nimesulide,on the growth of lung tumors and their expression of cyclooxygenase-2 and peroxisome proliferatoractivatedreceptor-γ [J]. Clinical Cancer Research, 2004, 10(4): 1521-1529.[9] Mestre J R, Rivadeneira D E, Mackrell P J, et al. Overlapping CRE and E-box promoer elements canindependently regulate COX-2 gene transcription in macrophages [J]. FEBS Letters, 2001, 496(2-3): 147-151.[10] Thomas B, Berenbaum F, Humbert L, et al. Critical role of C/EBPδ and C/EBPβ factors in the stimulationof the cyclooxygenas-2 gene transcription by interleukin-1β in articular chondrocytes [J]. EuropeanJournal of Biochemistry, 2000, 267: 6798-6808.[11] Baeuerle P A. IκB-NF-κB structure: At the interface of inflammation control [J]. Cell, 1998, 95: 729-731.[12] Jacobs M D, Harrison S C. Structure of an IκBα/NF-κB complex [J]. Cell, 1998, 95: 749-758.[13] Benitah S A, Valer′on P F, Lacal J C. ROCK and nuclear factor-κB-dependent activation ofcyclooxygenase-2 by rho GTPases: Effects on tumor growth and therapeutic consequences [J]. MolecularBiology of the Cell, 2003, 14(7): 3041-3054.[14] Wen D, Nong Y, Morgan J G, et al. A selective small molecule IκB kinase β inhibitor blocks nuclearfactor κB-mediated inflammatory responses in human fibroblast-like synoviocytes, chdrocytes, and mast cells[J]. Journal of Pharmacology and Experimental Therapeutics, 2006, 317(3): 989-1001.[15] Heiss E, Herhaus C, Klimo K, et al. Nuclear factor κB is a molecular target for sulforaphane-mediatedanti-inflammatory mechanisms [J]. Journal of Biological Chemistry, 2001, 276(34): 8-15.[16] Kaltschmidt B, Linker R A, Deng J, et al. Cyclooxygenae-2 is a neuronal target gene of NF-κB[J]. BMC Molecular Biology, 2002, 3: 16-27. |