[1] Kinoshita K, Sato K, Hori M, et al. Decrease in activity of smooth muscle L-type Ca2+ channels and its reversal by NF-kappaB inhibitors in Crohn’s colitis model [J]. Am J Physiol Gastrointest Liver Physiol, 2003, 285 (3):G483-93. [2] Monaco C, Andreakos E, Kiriakidis S, et al. Canonical pathway of nuclear factor κappa B activation selectively regulates proinflammatory and prothrombotic responses in human atherosclerosis [J].Proc Natl Acad Sci USA, 2004, 101(15): 5634-9. [3] LappasM, YeeK, PermezelM, et al. Sulphasalazine and BAY 11-7082 interfere with the NF-kappa B and IKK-beta pathway to regulate the release of pro-inflammatory cytokines from human adipose tissue and skeletal muscle, In Vitro [J]. Endocrinology,2004, [Epub chead of print]. [4] Jobin C, Bradham CA, Russo MP, et al. Curcumin blocks cytokinemediated NF-kappa B activation and proinflammatory gene expression by inhibiting inhibitory factor I-κ appa B kinase activity[J]. J Immunol, 1999,163(6):3474-83. [5] Neurath MF, Fuss I, Kelsall BL, et al. Antibodies to interleukin 12 abrogate established experimental colitis in mice [J]. J Exp Med,1995, 182(5): 1281-90. [6] Hugot JP, Chamaillard M, Zouali H, et al. Association of NOD2 leucine-rich repeat variants with susceptibility to Crohn’s disease[J]. Nature, 2001,411(6837):599-603. [7] Ogura Y, Bonen DK, Inohara N, et al. A frameshift mutation in NOD2 associated with susceptibility to Crohn’s disease [J]. Nature,2001, 411(6837): 603-6. [8] Ogura Y, Inohara N, Benito A, et al. Nod2, a Nod1/Apaf-1 family member that is restricted to monocytes and activates NF-kappaB [J].J Biol Chem, 2001, 276(7): 4812-8. [9] Monteleone G, Mann J, Monteleone I, et al. A failure oftransforming growth factor-betal negative regulation maintains sustained NF-κ appaB activation in gut inflammation[J]. J Biol Chem, 2004,279(6):3925-32. [10] Cui HH, Chen CL, Wang JD, et al. Effects of probiotic on intestinal mucosa of patients with ulcerative colitis [J]. World J Gastroenterol,2004, 10(10): 1521-5. [11] Ferretti M, Casini Raggi, Vpizarro TT, et al. Neutralization of endogenous IL1 receptor antagonist exacerbates and prolongs inf lammation in rabbit immune colitis [J]. J Clin Invest, 1994, 94(1):449-53. [12] Bickston S J, Cominelli F. Recombinant interleukin 10 for the treatment of active Crohn’s disease: lessons in biologic therapy [J].Gastroenterology, 2000, 119(6): 1781-3. [13] Shibata Y, Taruishi M, Ashida T. Experimental ileitis in dogs and colitis in rats with trinitrobenzene sulfonic acid--colonoscopic and histopathologic studies [J]. Gastroenterol Jpn, 1993, 28(4): 518-27. [14] Dijkstra G, Moshage H, Jansen PL. Blockade of NF-κ appaB activation and donation of nitric oxide: new treatment options in inflammatory bowel disease [J]? Scand J Gastroenterol Suppl, 2002,(236): 37-41. [15] Jobin C, Bradham CA, Russo MP, et al. Curcumin blocks cytokinemediated NF-kappa B activation and proinflammatory gene expression by inhibiting inhibitory factor I-κ appa B kinase activity[J]. J Immunol, 1999, 163(6): 3474-83. [16] Baldwin AS. The NF-κB and IκB proteins: new discoveries and insights [J].Annu Rev Immunol, 1996, 14: 649-83. |