Improvement effect of psoralen on intestinal barrier and secondary liver injury in mice with ulcerative colitis
This study aims to investigate the potential of psoralen(PSO)in ameliorating intestinal barrier dysfunction and secondary liver injury in mice with ulcerative colitis(UC).Forty male C57BL/6J mice were randomly assigned into the fol-lowing groups:control group(Con),model group(Mod),positive control group treated with sulfasalazine(SASP,200 mg/kg),low-dose PSO group(PSO-L,20 mg/kg),and high-dose PSO group(PSO-H,40 mg/kg).Ulcerative colitis(UC)mod-els were induced by freely drinking 2.25％dextran sulfate sodium salt(DSS)for seven days.During the experiment,the weight of mice and disease activity index(DAI)were recorded.Real-time quantitative polymerasechain reaction(RT-qPCR)was used to detect the expression of zonula occludens-1(ZO1),Claudin-1 and Occludin in the colon.Biochemical assay kits were employed to measure the levels of aspartate aminotransferase(AST),alanine transaminase(ALT),alkaline phosphatase(AKP)and lactate dehydrogenase(LDH)in the liver.Enzyme-linked immunosorbent assay(ELISA)was conducted to quantify the levels of lipopolysaccharides(LPS),C-reactive protein(CRP),procalcitonin(PCT),interleukin-6(IL-6)and tumor necrosis factor-alpha(TNF-α)in the liver.Western blot analysis was performed to assess the expression of Toll-like re-ceptor 4(TLR4),myeloid differentiation primary response protein 88(MyD88)and phosphorylated nuclear factor kappa-B(p-NF-κB)in the liver.The results showed that compared to the Mod group,after PSO treatment,the weight loss of UC mice was alleviated,DAI scores decreased,and colonic length shortening was relieved.The mRNA expression of ZOl,Claudin-l,and Occludin was upregulated.The levels of AST,ALT,AKP and LDH in the liver decreased;the levels of LPS,CRP,PCT,IL-6 and TNF-α in the liver decreased;and the expression of TLR4,MyD88 and p-NF-κB proteins in the liver was downregu-lated.The above results indicate that PSO can improve intestinal barrier function in DSS-induced mice and ameliorate second-ary liver injury by inhibiting the TLR4/MyD88/NF-κB signaling pathway.
万方数据
维普
