Conclusion
CMOS inhibit inflammation, alter intestinal barrier integrity, and regulate gut microbiota to attenuate AS in ApoE-/- mice.
Results
CMOS are supplemented in atherosclerotic male ApoE-/- mice fed with a high-fat-high-cholesterol diet (HFHCD). After the 12-week intervention, CMOS at 1200 mg kg-1 ·bw d-1 significantly decrease the atherosclerotic lesion area by 0.63-fold and the aortic arch lesion size by 0.63-fold when compared to the HFHCD group. Moreover, inflammation in atherosclerotic lesions is reduced by CMOS intervention, and the levels of serum lipids and inflammatory cytokines are decreased. The number of goblet cells and the expression of intestinal epithelial tight junction proteins in the H-CMOS group increase, thus indicating that CMOS can restore intestinal barrier integrity in atherosclerotic mice. Furthermore, CMOS reshape the unbalanced gut microbiota in ApoE-/- mice caused by HFHCD, and reduce the relative abundance of Desulfovibrio and Faecalibaculum that exhibits positive relationships with inflammation.