Abstract
Dysfunction of energy metabolism is involved in inflammatory bowel disease (IBD). This study was designed to investigate the potential of astragaloside IV (ASIV), an active ingredient of Radix Astragalus, to ameliorate colonic mucosal injury, with focusing on the implication of energy restoration in the underlying mechanism. Experimental colitis model was established in rats by injecting 2,4,6-trinitrobenzene sulfonic acid (TNBS) through anus. After 24 hours, ASIV was administrated once daily by gavage for 6 days. On day 1 and day 7, colon tissue was collected for macroscopic and histological examination, ELISA, Western blot and immunohistochemical analysis. TNBS impaired colonic mucosa with an injured epithelial architecture, increased inflammatory cell infiltration, and decreased colonic blood flow. Lgr5 positive cell number in crypt and β-catenin nuclear translocation were down-regulated by TNBS treatment. TNBS induced epithelial F-actin disruption and junctional protein degradation. Furthermore, adenosine triphosphate (ATP) content and ATP synthase subunit β expression in the colon tissue were significantly decreased after TNBS stimulation. All of the aforementioned alterations were relieved by ASIV post-treatment. The present study revealed that ASIV promoted mucosal healing process in TNBS-induced colitis, which was most likely attributed to regulating energy metabolism.
Highlights
Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), is an idiopathic disease characterized by chronic, relapsing inflammation and erosion as well as ulcer in the gastrointestinal tract with increased risk of developing colorectal cancer[1,2]
We first evaluated the efficacy of astragaloside IV (ASIV) in coping with colitis in rats, which were challenged by trinitrobenzene sulfonic acid (TNBS) for 24 hours followed by treatment with ASIV for 6 days
Sham: sham group; ASIV: ASIV alone group; TNBS 1D: TNBS treatment for 1 day group; TNBS 7D: TNBS treatment for 1 days followed by saline treatment for 6 days group; TNBS 7D +ASIV: TNBS treatment for 1 day followed by ASIV treatment for 6 days group
Summary
Inflammatory bowel disease (IBD), which includes ulcerative colitis (UC) and Crohn’s disease (CD), is an idiopathic disease characterized by chronic, relapsing inflammation and erosion as well as ulcer in the gastrointestinal tract with increased risk of developing colorectal cancer[1,2]. In a variety of human diseases, including IBD as well as colon cancer, this renewal process is dysregulated and the homeostasis in the intestinal epithelium is www.nature.com/scientificreports/. Dysfunction of energy metabolism has been shown to be implicated in the pathogenesis of IBD11 Inflammation reaction, such as neutrophils infiltration and phagocytosis, increases the demand of energy. Inflammation-induced abnormal microvasculature causes a decreased supply of nutrient and oxygen that further aggravates the energy deficiency. This energy deficiency contributes to the disruption of mucosal epithelium barrier found in IBD, which is regulated by interendothelial cell junctions and F-actin filaments, both of which need energy to maintain integrity[12,13,14]. Regulating energy metabolism is anticipated as a promising strategy for IBD therapy
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