Protective effect of sugar cane extract against dextran sulfate sodium-induced colonic inflammation in mice. Issue 1 (February 2017)

• Record Type: Journal Article
• Authors: Wang, Bin; Li, Yansen; Mizu, Masami; Furuta, Toma; Li, ChunMei
• Is Part Of: Tissue & cell. Volume 49:Issue 1(2017)
• Page Start: 8
• Page End: 14
• Publication Date: 2017-02
• Subjects: SCE sugar cane extract -- DSS dextran sulfate sodium -- Nrf2 nuclear factor E2-related factor 2 -- CAT catalase -- SOD1 superoxide dismutase 1 -- Gpx1 glutathione peroxidase 1 -- Gpx4 glutathione peroxidase 4 -- TNF-α tumor necrosis factor-alpha -- GSH-PX glutathione peroxidase -- MDA malondialdehyde -- T-AOC total antioxidant capability -- ZO-1 zona occludens-1 -- IBD inflammatory bowel disease; Sugar cane extract -- Inflammation -- Oxidative stress -- Tight junction -- Mouse; Cytology -- Periodicals; 571.5
• DOI: 10.1016/j.tice.2016.12.008
• Languages: English
• ISSNs: 0040-8166

Abstract

Highlights: SCE improved growth performance and spleen relative weight in the DSS-induced inflammation. SCE upregulated the colonic SOD1 expression. SCE alleviated DSS-disturbed tight junctions and the DSS-induced inflammation. SCE ameliorated the DSS-promoted effect on the p65 nuclear accumulation and the DSS-inhibited effect on the Nrf2 nuclear accumulation. Abstract: Sugar cane extract (SCE) exhibits various biological effects and has been reported to enhance animal growth performance. However, the effect of SCE on inflammation in animals is still obscure. To study the effects and underlying mechanism of SCE on dextran sulfate sodium (DSS)-induced colonic inflammation, forty female ICR mice (26.63 ± 0.19 g, 6-week-old) were assigned into four groups: a control group (Cont), a DSS-challenged group (DSS), a SCE-supplemented group (SCE), and a DSS+SCE group (DSS+SCE). Mice in Cont group and DSS group were fed basic diet and other mice received 1% SCE supplemented in basic diet from 6-week to 8-week-old. Mice in DSS and DSS+SCE groups were also given a 4% DSS solution from 7-week to 8-week-old via drinking water to induce colonic inflammation. After 2 weeks, mice were sacrificed and samples were collected. The results showed that dietary SCE alleviated DSS induced growth suppression, splenic damage, colonic histological changes, colonic inflammation, oxidative stress, and colonic dysfunction of tight junctions. Meanwhile, the DSS exposure activated nuclear transcription factor kappa B p65 and inhibited nuclear factor E2-related factor 2 (Nrf2), while SCE markedly attenuated the DSS-promoted effect on the p65 nuclear accumulation and the DSS-inhibited effect on the Nrf2 nuclear accumulation. In conclusion, SCE conferred a protective role in the DSS-induced inflammation and the mechanism might be associated with the activated signals of the nuclear factor kappa B p65 and Nrf2.