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Journal of environmental pathology, toxicology and oncology : official organ of the International Society for Environmental Toxicology and Cancer 2014

Protective effect of Acacia ferruginea against ulcerative colitis via modulating inflammatory mediators, cytokine profile and NF-κB signal transduction pathways.

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Kunnathur Murugesan Sakthivel
Chandrasekaran Guruvayoorappan

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概要

In the present study, we evaluated the protective effect of A. ferruginea extract against ulcerative colitis (UC). Male Wistar rats received A. ferruginea extract (10 mg/kg body weight) or sulfasalazine (100 mg/kg body weight) for 5 consecutive days before inducing UC via intrarectal acetic acid (3%) administration. Colonic mucosal injury was assessed by macroscopic scoring, vascular permeability testing, and histopathological examination. The mucosal contents of glutathione, lipid peroxidation, superoxide dismutase, and nitric oxide were evaluated as parameters for the redox state. Inflammatory response was determined by measuring inducible nitric oxide synthase (iNOS) and cyclo-oxygenase (COX-2) expression. Myeloperoxidase (MPO), lactate dehydrogenase assay (LDH), tumor necrosis factor (TNF-α), and interleukins (IL-1β and IL-6) were measured using ELISA. Transcription factor profiling of nuclear factor (NF)-κB subunits (p65/p50) was also conducted using ELISA. All of the relevant parameters were altered in rats with UC, and these parameters improved in animals that received A. ferruginea extract. Colonic mucosal injury parallels antioxidant and anti-inflammatory evaluations, and A. ferruginea extract was considered comparable to the standard treatment drug sulfasalazine. Histopathological studies confirmed these findings. A. ferruginea extract inhibited the activation and translocation of transcription factors, that is, NF-κB subunits (p65/p50). The results of our investigation clearly indicate that treatment with A. ferruginea extract exerted a marked protective effect against experimental UC via modulation of oxidant/anti-oxidant balance and inhibition of inflammatory mediators.

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