%0 Journal Article
%T A Picrorhiza kurroa Derivative, Picroliv, Attenuates the Development of Dextran-Sulfate-Sodium-Induced Colitis in Mice
%A De-Kui Zhang
%A Jian-Jie Yu
%A Yu-Min Li
%A Li-Na Wei
%A Yi Yu
%A Yan-Hu Feng
%A Xiang Wang
%J Mediators of Inflammation
%D 2012
%I Hindawi Publishing Corporation
%R 10.1155/2012/751629
%X Background. Free radicals and proinflammatory cytokines have been shown to play a critical role in the pathogenesis of ulcerative colitis (UC). Picroliv, a Picrorhiza kurroa derivative, has been demonstrated to have antioxidant and anti-inflammatory effect. The purpose of the study was to investigate the effects of picroliv on experimental model of UC in mice. Materials and Methods. Picroliv was administrated orally by gavage to mice with colitis induced by dextran sulfate sodium (DSS). Disease activity index (DAI), colon length, and histology score were observed. Myeloperoxidase (MPO) activity, and SOD, MDA concentrations were measured by enzyme-linked immunosorbent assay (ELISA) while the expression of cytokine mRNAs was studied by real-time-quantitative polymerase chain reaction and also ELISA. The expression of NF-¦ÊB p65 was observed by immunohistochemistry staining and western blotting. Results. A significant improvement was observed in DAI and histological score in mice treated with picroliv, and incerased MPO activity, MDA concentrations, and the expression of IL-1¦Â, TNF-¦Á, and NF-¦ÊB p65 in mice with DSS-induced colitis were significantly reduced while decreased SOD level increased following administration of picroliv. Conclusion. The administration of picroliv leads to an amelioration of DSS-induced colitis, suggesting administration of picroliv may provide a therapeutic approach for UC. 1. Introduction Ulcerative colitis (UC) is a chronic inflammatory bowel disease of unknown cause that exhibits an unpredictable clinical course with remissions and exacerbation and is characterized by rectal bleeding and diarrhea [1]. Although great advances have been made in the management of the disease, no definitive therapies until now are available for this disorder because the exact pathogenesis is elusive [2, 3]. Conventional treatments for UC include aminosalicylates and corticosteroids as mainstays of therapy. Immunosuppressive agents, such as azathioprine, 6-mercaptopurine, and methotrexate, are used for corticosteroid-resistant or -dependent patients. However, these drugs are not always effective and may inflict serious side effects [2¨C4]. Recently, a biologic agent, antitumor necrosis factor alpha (anti-TNF- ) antibody (infliximab), has been shown to be effective in clinical application; however, infliximab can cause serious adverse reactions such as increased risk of infection, hypersensitivity, and anti-antibody reaction and an unknown risk of mutagenesis [5, 6]. Therefore, new therapeutic strategies are awaited. Although the precise mechanism of
%U http://www.hindawi.com/journals/mi/2012/751629/