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Bletilla striata polysaccharides ameliorates lipopolysaccharide-induced injury in intestinal epithelial cells
BACKGROUND/AIMS: This study was carried out to investigate the effect of Bletilla striata polysaccharide (BSP) treating on lipopolysaccharide (LPS)-induced intestinal epithelial barrier disruption in rat intestinal epithelial cell (IEC) line. MATERIALS AND METHODS: LPS was used to stimulate the IEC-...
Autores principales: | , , , , , , |
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Formato: | Online Artículo Texto |
Lenguaje: | English |
Publicado: |
Wolters Kluwer - Medknow
2019
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Materias: | |
Acceso en línea: | https://www.ncbi.nlm.nih.gov/pmc/articles/PMC6784437/ https://www.ncbi.nlm.nih.gov/pubmed/31044747 http://dx.doi.org/10.4103/sjg.SJG_520_18 |
Sumario: | BACKGROUND/AIMS: This study was carried out to investigate the effect of Bletilla striata polysaccharide (BSP) treating on lipopolysaccharide (LPS)-induced intestinal epithelial barrier disruption in rat intestinal epithelial cell (IEC) line. MATERIALS AND METHODS: LPS was used to stimulate the IEC-18 cells (1 μg/ml), with or without different concentrations of BSP (25, 50 and 100 μg/ml) for 24 h. Transepithelial electrical resistance (TEER) was measured to detect the permeability of cells. Interleukin-6 (IL-6) and tumor necrosis factor-α (TNF-α) in the cell supernatant were detected with the enzyme-linked immunosorbent assay (ELISA). Real-time polymerase chain reaction (PCR) was employed to detect the mRNA levels of zonulae occludens (ZO)-1 and occludin. Western blot and immunofluorescence analysis were used for analyzing the expression level and the distribution patterns of ZO-1 and occludin protein. RESULTS: After treatment with BSP, the IL-6 and TNF-α levels in the cell supernatant were significantly decreased compared with the experiment group (P < 0.05 or 0.01). The permeability of IEC was decreased in BSP groups when compared with the experiment group (P < 0.05 or 0.01). In addition, compared with the experiment group, treatment with BSP up-regulated mRNA and protein expression levels of ZO-1 and occludin, and kept the ZO-1 and occludin protein intact in IEC-18 cells injured with LPS (P < 0.05 or 0.01). CONCLUSION: BSP has the capacity to protect IEC-18 cells from LPS-induced injury. The mechanisms may be associated with decreasing the inflammatory cytokine levels of IL-6 and TNF-α, and elevating the expression of ZO-1 and occludin, which might serve as a new protective agent for LPS-induced intestinal epithelial barrier disruption. |
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