cytellin and Colitis

In this article, we aim to examine the novel effects of β-sitosterol on murine experimental colitis. β-Sitosterol significantly reduces the weight loss, colon length, and alleviated microscopic appearances of colitis induced by dextran sulfate sodium. This compound also decreases the levels of TNF-α, IL-6, and IL-1β in intestinal tissue of mice with experimental colitis in a concentration-dependent manner. β-Sitosterol treatment to intestinal epithelial cells significantly increases expression of antimicrobial peptides and reduces survival of intracellular Salmonella typhimurium. These results showed the multiple effects of β-sitosterol against pathogenic bacteria for a novel approach to the treatment of colonic inflammation.

Topics: Animals; Colitis; Dextran Sulfate; Disease Models, Animal; Hypolipidemic Agents; Inflammation; Intestinal Mucosa; Male; Mice; Mice, Inbred C57BL; Salmonella typhimurium; Sitosterols; Typhoid Fever

The effects of daucosterol have been identified in cancer therapy and neuronal diseases. However, the regulatory function of daucosterol in DSS-induced colitis has not yet been investigated. In this study, we evaluated the immunological and therapeutic effects of daucosterol in a mouse model of dextran sulfate sodium (DSS)-induced colitis. Unlike vehicle mice, mice pre- or post-treated with daucosterol showed inhibition of body weight loss and the decrease in the disease activity index (DAI). In addition, daucosterol treatment rescued the DSS-induced decrease in colon length and disruption of the epithelial lining. Furthermore, it reduced DSS-induced production of reactive oxygen species (ROS), infiltration of macrophages, and expression of pro-inflammatory cytokines such as TNF-α, IL-6, and IL-1β. Mice with colitis showed a decreased population of Foxp3

Topics: Animals; Anti-Inflammatory Agents; Colitis; Colon; Cytokines; Dextran Sulfate; Female; Killer Cells, Natural; Lymph Nodes; Mice, Inbred C57BL; Sitosterols; Spleen; T-Lymphocytes, Regulatory

Phytosterols, the plant analogues of cholesterol, widely occur in the human diet. In this study, we investigated and compared the effects of stigmasterol and β-sitosterol (both with purities ≥95%) on dextran sulfate sodium (DSS)-induced colitis in C57BL/6J male mice fed a high fat Western-style diet. Mice treated with DSS developed severe mucosal colitis, with a marked distortion and crypt loss of colonic surface epithelium. Both β-sitosterol and stigmasterol significantly inhibited colon shortening, lowered fecal hemoglobin content, and reduced the severity of colitis in the middle and distal colon (p < 0.05). These phytosterols also significantly suppressed the activation of nuclear factor-kappa B. They also significantly decreased colony stimulating factor-1 and the nuclear translocation of inflammatory master regulator nuclear factor-kappa B. Stigmasterol significantly lowered the colonic inflammation score and the expression of cyclooxygenase-2 and colony stimulating factor-1, while β-sitosterol was less or not effective. These results suggest that dietary intake of stigmasterol and β-sitosterol ameliorates colitis. Such activities of stigmasterol and β-sitosterol in humans remain to be investigated.

Topics: Animals; Colitis; Dextran Sulfate; Diet, High-Fat; Humans; Male; Mice; Mice, Inbred C57BL; Sitosterols; Stigmasterol

In this study, we evaluated the effects of dietary plant sterols and stanols as their fatty acid esters on the development of experimental colitis. The effects were studied both in high- and low-fat diet conditions in two models, one acute and another chronic model of experimental colitis that resembles gene expression in human inflammatory bowel disease (IBD). In the first experiments in the high fat diet (HFD), we did not observe a beneficial effect of the addition of plant sterols and stanols on the development of acute dextran sulphate sodium (DSS) colitis. In the chronic CD4CD45RB T cell transfer colitis model, we mainly observed an effect of the presence of high fat on the development of colitis. In this HFD condition, the presence of plant sterol or stanol did not result in any additional effect. In the second experiments with low fat, we could clearly observe a beneficial effect of the addition of plant sterols on colitis parameters in the T cell transfer model, but not in the DSS model. This positive effect was related to the gender of the mice and on Treg presence in the colon. This suggests that especially dietary plant sterol esters may improve intestinal inflammation in a T cell dependent manner.

Topics: Acute Disease; Animals; Anti-Inflammatory Agents; Antigens, CD; Brassica rapa; Chronic Disease; Colitis; Colon; Diet, Fat-Restricted; Diet, High-Fat; Dietary Fats; Esters; Fatty Acids; Fatty Acids, Monounsaturated; Female; Inflammation; Inflammatory Bowel Diseases; Male; Mice, Inbred C57BL; Phytosterols; Phytotherapy; Plant Oils; Rapeseed Oil; Sitosterols; T-Lymphocytes

β-Sitosterol, a common phytosterol, has been shown to exhibit anti-inflammatory effects. Here, we investigated the effect of β-sitosterol on high-fat diet (HFD) induced colitis in mice and on LPS-stimulated mouse intestinal macrophages.. C57BL/6J mice were maintained on an LFD (10 kcal% fat), an HFD (60 kcal% fat), or an HFD with β-sitosterol (20 mg/kg) administration for 8 weeks. The increased levels of body weight and epididymal fat pad weight as well as the concentrations of circulating proinflammatory cytokines and LPS in HFD mice compared with LFD mice were decreased by oral administration of β-sitosterol. The HFD-induced colonic inflammation evidenced by the increased expression of proinflammatory cytokines and the activation of nuclear factor kappa B (NF-κB) in the colon was also inhibited by β-sitosterol. In LPS-stimulated intestinal macrophages, β-sitosterol inhibited the production of proinflammatory cytokines and inflammatory enzymes as well as NF-κB activation. In addition, β-sitosterol significantly prevented the binding of LPS to intestinal as well as peritoneal macrophages. Furthermore, β-sitosterol potently inhibited the interaction between LPS and toll-like receptor 4 in intestinal macrophages transfected with control siRNA or MyD88 siRNA.. These findings indicate that β-sitosterol ameliorates HFD-induced colitis by inhibiting the binding of LPS to toll-like receptor 4 in the NF-κB pathway.

Topics: Animals; Colitis; Cytokines; Diet, High-Fat; Inflammation; Intestines; Lipopolysaccharides; Macrophages, Peritoneal; Male; Mice; Mice, Inbred C57BL; Mice, Inbred ICR; Myeloid Differentiation Factor 88; NF-kappa B; RNA, Small Interfering; Signal Transduction; Sitosterols; Toll-Like Receptor 4

β-Sitosterol, a common sterol in herbal medicines, exhibits anti-inflammatory effects beneficial in the treatment of lung inflammation, asthma, and bronchospasm. To evaluate whether β-sitosterol also has anticolitic benefits, we tested the effect of β-sitosterol on 2,4,6-trinitrobenzene sulfonic acid (TNBS)-induced colitis in mice. β-Sitosterol inhibited colon shortening and led to lowered macroscopic scores and myeloperoxidase activity in TNBS-treated colitic mice. β-Sitosterol also inhibited the expression of proinflammatory cytokines TNF-α, IL-1β, and IL-6, and an inflammatory enzyme, cyclooxygenase (COX)-2, in the colons of TNBS-induced colitic mice, as well as the activation of NF-κB. Based on these findings, β-sitosterol may ameliorate colitis by inhibiting the NF-κB pathway.

Topics: Animals; Colitis; Cyclooxygenase 2; Interleukin-1beta; Interleukin-6; Male; Mice; Mice, Inbred C57BL; NF-kappa B; Peroxidase; Sitosterols; Trinitrobenzenesulfonic Acid; Tumor Necrosis Factor-alpha