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Buckwheat and buckwheat enriched products exert an anti-inflammatory effect on the myofibroblasts of colon CCD-18Co.

ABSTRACT: Buckwheat (BW) constitutes a good source of bioactive components that show anti-inflammatory effects in vitro and in vivo. The use of functional foods in the prevention and treatment of inflammatory bowel diseases (IBDs) has aroused increasing interest. This study investigates the effect of in vitro digested BW and BW-enriched products (BW-enriched wheat breads, roasted BW groats -fermented and non-fermented-, and BW sprouts) on colon myofibroblasts, the cells involved in the regulation of inflammatory response in the intestine. The cells were treated with different digested-BW products, alone or together with TNF-? (20 ng mL-1), and the effects on the cell migration, mitochondrial membrane potential and cell cycle, processes altered during intestinal inflammation, were investigated. A significant reduction in TNF-?-induced migration (25.5%, p < 0.05) and attenuation of the TNF-?-altered cell cycle (p < 0.05) was observed in myofibroblasts treated with BW-enriched white wheat bread. These results contribute to extend the beneficial effects derived from BW bioactive compounds, and suggest that BW consumption can exert beneficial effects on IBDs.

SUBMITTER: Gimenez-Bastida JA

PROVIDER: S-EPMC6597957 | biostudies-literature | 2018 Jun

REPOSITORIES: biostudies-literature

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Buckwheat and buckwheat enriched products exert an anti-inflammatory effect on the myofibroblasts of colon CCD-18Co.

Giménez-Bastida J A JA Laparra-Llopis J M JM Baczek N N Zielinski H H

Food & function 20180601 6

Buckwheat (BW) constitutes a good source of bioactive components that show anti-inflammatory effects in vitro and in vivo. The use of functional foods in the prevention and treatment of inflammatory bowel diseases (IBDs) has aroused increasing interest. This study investigates the effect of in vitro digested BW and BW-enriched products (BW-enriched wheat breads, roasted BW groats -fermented and non-fermented-, and BW sprouts) on colon myofibroblasts, the cells involved in the regulation of infla ...[more]

PMID: 29870039

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Project description:BackgroundIntestinal fibrosis is a serious complication of inflammatory bowel disease, including Crohn's disease and ulcerative colitis. There is no specific treatment for intestinal fibrosis. Studies have indicated that peroxisome proliferator-activated receptor- γ (PPAR-γ) agonists have anti-fibrogenic properties in organs besides the gut; however, their effects on human intestinal fibrosis are poorly understood. This study investigated the anti-fibrogenic properties and mechanisms of PPAR-γ agonists on human primary intestinal myofibroblasts (HIFs).MethodsHIFs were isolated from normal colonic tissue of patients undergoing resection due to colorectal cancer. HIFs were treated with TGF-β1 and co-incubated with or without one of two synthetic PPAR-γ agonists, troglitazone or rosiglitazone. mRNA and protein expression of procollagen1A1, fibronectin, and α-smooth muscle actin were determined by semiquantitative reverse transcription-polymerase chain reaction and Western blot. LY294002 (Akt inhibitor) was used to examine whether Akt phosphorylation was a downstream mechanism of TGF-β1 induced expression of procollagen1A1, fibronectin, and α-smooth muscle actin in HIFs. The irreversible PPAR-γ antagonist GW9662 was used to investigate whether the effect of PPAR-γ agonists was PPAR-γ dependent.ResultsBoth PPAR-γ agonists reduced the TGF-β1-induced expression of α-smooth muscle actin which was integrated into stress fibers in HIFs, as determined by actin microfilaments fluorescent staining and α-smooth muscle actin-specific immunocytochemistry. PPAR-γ agonists also inhibited TGF-β1-induced mRNA and protein expressions of procollagen1A1, fibronectin, and α-smooth muscle actin. TGF-β1 stimulation increased phosphorylation of downstream signaling molecules Smad2, Akt, and ERK. TGF-β1 induced synthesis of procollagen1A1, fibronectin, and α-smooth muscle actin through a phosphatidylinositol 3-kinase/Akt-dependent mechanism. PPAR-γ agonists down regulated fibrogenesis, as shown by inhibition of Akt and Smad2 phosphorylation. This anti-fibrogenic effect was PPAR-γ independent.ConclusionsTroglitazone and rosiglitazone suppress TGF-β1-induced synthesis of procollagen1A1, fibronectin, and α-smooth muscle actin in HIFs and may be useful in treating intestinal fibrosis.

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Buckwheat and buckwheat enriched products exert an anti-inflammatory effect on the myofibroblasts of colon CCD-18Co.

Publications

Buckwheat and buckwheat enriched products exert an anti-inflammatory effect on the myofibroblasts of colon CCD-18Co.

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