Bletilla striata polysaccharides ameliorates lipopolysaccharide-induced injury in intestinal epithelial cells
Lei Luo1, Yuqing Liu2, Xin Cai2, Yao Wang3, Juan Xue4, Juan Zhang5, Fan Yang6
1 Department of Gastroenterology, The Second People's Hospital of China Three Gorges University, Yichang, P.R. China
2 School of Clinical Medical, Hubei University of Chinese Medicine, Wuhan, P.R. China
3 Department of Infectious Diseases, Renmin Hospital of Wuhan University, Wuhan, P.R. China
4 Department of Gastroenterology, Hubei Provincial Hospital of Traditional Chinese and Western Medicine, Wuhan, P.R. China
5 Department of Pulmonary Diseases, Jingmen City Hospital of Traditional Chinese Medicine, Jingmen, P.R. China
6 Department of Hepatology, Hubei Provincial Hospital of Chinese Medicine, Wuhan, P.R. China
Dr. Fan Yang
Department of Hepatology, Hubei Provincial Hospital of Chinese Medicine, 856 Luoyu Road, Hongshan District, Wuhan - 430074
Source of Support: None, Conflict of Interest: None
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.