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      Anti-Inflammatory Effects of an Extract of Polygonum hydropiper Stalks on 2,4,6-Trinitrobenzenesulphonic Acid-Induced Intestinal Inflammation in Rats by Inhibiting the NF- κB Pathway

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          Abstract

          The stalks of Polygonum hydropiper L. (PHL) have been traditionally used in clinical practice for thousands of years in China to treat various inflammatory diseases. However, little research has been conducted to investigate the anti-inflammatory effects of PHL on TNBS-induced intestinal inflammation in rats. The aim of the present study was to investigate the anti-inflammatory effects and to explain the underlying mechanism of PHL on TNBS-induced intestinal inflammation in rats. PHL (125, 250, and 500 mg/kg) was given for 7 consecutive days to rats with intestinal inflammation induced by TNBS. Oral administration of an aqueous extract of a high dose of PHL (H- PHL) significantly improved TNBS-induced symptoms such as the macroscopic score and histological examination. H- PHL treatment significantly ameliorated the activity of MPO and improved the GSH content. In addition, there was a downregulation of the TNBS-induced increase in the activity of iNOS and levels of Cox-2, TNF- α, and IL-1 β while the protein expression of NF- κB was significantly unregulated after administration of H- PHL. The present findings suggested that H- PHL has a protective effect on experimental intestinal inflammation in rats and its anti-inflammatory effects are closely related to inhibition of NF- κB signal pathways.

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          Most cited references52

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          NF-kappaB in inflammatory bowel disease.

          Apart from genetic and environmental factors, the mucosal immune system of the gut plays a central role in the pathogenesis of inflammatory bowel disease (IBD). In the healthy gut, the mucosal immune system ensures the balance between pro- and anti-inflammatory mediators and thereby allows an effective defence against luminal pathogens but at the same time prevents an overwhelming immune reaction directed against the huge amount of harmless luminal antigens (for example, components of food or nonpathological bacteria). In both entities of IBD (Crohn's disease and ulcerative colitis) this immunological balance is severely impaired and shifted towards the pro-inflammatory side. The chronic mucosal inflammation in IBD is caused by hyperactivation of effector immune cells, which produce high levels of pro-inflammatory cytokines like tumour necrosis factor-alpha, interleukin-6 and interferon-gamma, resulting in colonic tissue damage. The nuclear transcription factor kappaB (NF-kappaB) was identified as one of the key regulators in this immunological setting. Its activation is markedly induced in IBD patients and through its ability to promote the expression of various pro-inflammatory genes, NF-kappaB strongly influences the course of mucosal inflammation. Considering the different cell-type specific effects which are mediated by NF-kappaB, this review aims at describing the complex role of NF-kappaB in IBD and discusses existing pharmacological attempts to block the activation of NF-kappaB to develop new therapeutic strategies in IBD.
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            Hapten-induced model of chronic inflammation and ulceration in the rat colon.

            We have developed a simple and reproducible rat model of chronic colonic inflammation by the intraluminal instillation of a solution containing a "barrier breaker" and a hapten. Administration of the hapten 2,4,6-trinitrobenzenesulfonic acid (5-30 mg) in 0.25 ml of 50% ethanol as the "barrier breaker" produced dose-dependent colonic ulceration and inflammation. At a dose of 30 mg, trinitrobenzenesulfonic acid/ethanol-induced ulceration and marked thickening of the bowel wall persisted for at least 8 wk. Histologically, the inflammatory response included mucosal and submucosal infiltration by polymorphonuclear leukocytes, macrophages, lymphocytes, connective tissue mast cells, and fibroblasts. Granulomas were observed in 57% of the rats killed 3 wk after induction of inflammation. Langhan's-type giant cells were also observed. Segmental ulceration and inflammation were common. The characteristics and relatively long duration of inflammation and ulceration induced in this model afford an opportunity to study the pathophysiology of colonic inflammatory disease in a specifically controlled fashion, and to evaluate new treatments potentially applicable to inflammatory bowel disease in humans.
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              Glutathione and its role in cellular functions.

              H Sies (1999)
              Glutathione (GSH) is the major cellular thiol participating in cellular redox reactions and thioether formation. This article serves as introduction to the FRBM Forum on glutathione and emphasizes cellular functions: What is GSH? Where does it come from? Where does it go? What does it do? What is new and noteworthy? Research tools, historical remarks, and links to current trends.
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                Author and article information

                Contributors
                Journal
                Mediators Inflamm
                Mediators Inflamm
                MI
                Mediators of Inflammation
                Hindawi
                0962-9351
                1466-1861
                2018
                7 May 2018
                : 2018
                : 6029135
                Affiliations
                1School of Traditional Chinese Materia Medica, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang, Liaoning 110016, China
                2School of Pharmacy, Shenyang Pharmaceutical University, 103 Wenhua Road, Shenyang, Liaoning 110016, China
                Author notes

                Academic Editor: Julio Galvez

                Author information
                http://orcid.org/0000-0002-8320-2075
                Article
                10.1155/2018/6029135
                5964420
                29853790
                5267cf64-4880-4f2d-91c8-62a6de1b3f1b
                Copyright © 2018 Wei Zhang et al.

                This is an open access article distributed under the Creative Commons Attribution License, which permits unrestricted use, distribution, and reproduction in any medium, provided the original work is properly cited.

                History
                : 16 October 2017
                : 6 February 2018
                : 11 March 2018
                Funding
                Funded by: Project of Science and Technology of the Education Department of Liaoning Province
                Award ID: 2017LQN11
                Funded by: National Natural Science Foundation Committee of China
                Award ID: 81773879
                Award ID: 81470176
                Categories
                Research Article

                Immunology
                Immunology

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