Examination of the Anti-Inflammatory, Antioxidant, and Xenobiotic-Inducing Potential of Broccoli Extract and Various Essential Oils during a Mild DSS-Induced Colitis in Rats
Phytogenic compounds with antioxidant and anti-inflammatory properties are currently discussed as promising complementary agents in prevention and treatment of inflammatory bowel disease (IBD). Our study aimed to evaluate possible protective and curative effects of broccoli extract (BE) and of the essential oils of turmeric (Cuo), thyme (To), and rosemary (Ro) in a rat model with a mild dextran sulphate sodium- (DSS-) induced colitis. Therefore Wistar rats were fed a diet without an additive (Con) or diets with the addition of BE, Cuo, To, and Ro during the whole experiment. Pretreatment with Ro, Cuo, and To increased the expression of the tight junction protein Cldn3. All additives reduced mRNA of VCAM-1 which plays a crucial role in the first state of inflammatory response. Only Ro pretreatment affected the expression of the antioxidant enzymes HO1, GPx2, and of glutathione-S-transferases. All additives counteracted the DSS-induced rise in COX2 and VCAM-1 expression. Colonic IL-10 was increased by Cuo, To, and Ro. During the recovery phase DSS pretreatment increased NFκB, VCAM-1, and MCP-1: This response was counter-regulated by all additives. We conclude that the phytogenic additives tested have a promising anti-inflammatory potential in vivo and a particular role in the prevention of IBD. 1. Introduction Inflammatory bowel disease, including ulcerative colitis (UC) and Crohn’s disease (CD), is a multifactorial relapsing-remitting disorder, characterized by intermittent periods of acute inflammation in the small and in the large intestine. The main difference between CD and UC is the location and the nature of the inflammatory changes. CD can affect any part of the gastrointestinal tract, from mouth to anus, although the onset of the majority of cases is located in the terminal ileum. In contrast UC is restricted to the colon and the rectum. The exact pathogenic mechanisms provoking both disorders remain almost unclear. However, in a number of cases overreactions of the immune system due to inflammatory stimuli can be observed. In this context, proinflammatory immune modulators like interleukin 1 beta (IL-1β), monocyte chemoattractant protein 1 (MCP-1), and vascular cell adhesion molecule 1 (VCAM-1) play an important role in the development of the disease [1, 2]. Nuclear factor “kappa-light-chain-enhancer” of activated B cells (NFκB) represents a key transcription factor regulating the synthesis of genes involved in immune reactions and inflammatory response. In noninflamed tissues NFκB is inhibited through linkage to its cytosolic inhibitor protein
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