Mechanism of Fushen Granule on improving intestinal epithelial barrier injury / 中草药

ABSTRACT

Objective: To investigate the protection mechanism of Fushen Granule on LPS-induced intestinal epithelial cell (IEC-6) barrier injury. Methods: IEC-6 were divided into control group, model group, Fushen granule group, and p38MAPK inhibitor group. In addition to the control group, 1 μg/mL LPS was added to the other groups, 10% drug-containing serum and 10 μmol/L SB203580 were respectively added to the administration group. The apoptosis of IEC-6 were detected by flow cytometry; The permeability and transmembrane resistance of IEC-6 barrier were detected by Transwell assay; The mRNA levels of ICAM-1 and IL-1β were assessed by Real-time PCR; The expressions of occludin, ZO-1, p38MAPK, and DUSP1 were detected by western blotting. Results: Compared with the control group, the apoptosis of IEC-6 were significantly increased in model group (P < 0.01), the levels of ICAM-1 and IL-1β were significantly increased (P < 0.01), the occludin and ZO-1 were significantly decreased (P < 0.01), the intestinal permeability was significantly increased (P < 0.05), the mRNA levels of ICAM-1 and IL-1β in IEC-6 were significantly inhibited, the permeability of intestinal mucosal barrier was reduced (P < 0.05), the expressions of DUSP1, occludin and ZO-1were increased (P < 0.05, 0.01), the expression of p38MAPK was inhibited (P < 0.01), which showed a similar effect with p38MAPK inhibitor. Conclusion: Fushen Granule could regulate DUSP1 which inhibits the activation of p38MAPK signaling pathway, up-regulate Occludin and ZO-1, improve the tight junction of IEC-6, thereby improving the cell barrier function damage caused by LPS.