| First Author | Yasueda A | Year | 2020 |
| Journal | Sci Rep | Volume | 10 |
| Issue | 1 | Pages | 9972 |
| PubMed ID | 32561763 | Mgi Jnum | J:293796 |
| Mgi Id | MGI:6451867 | Doi | 10.1038/s41598-020-65306-4 |
| Citation | Yasueda A, et al. (2020) Sanguisorba officinalis L. derived from herbal medicine prevents intestinal inflammation by inducing autophagy in macrophages. Sci Rep 10(1):9972 |
| abstractText | Disturbed activation of autophagy is implicated in the pathogenesis of inflammatory bowel disease. Accordingly, several autophagy-related genes have been identified as Crohn's disease susceptibility genes. We screened the autophagy activators from a library including 3,922 natural extracts using a high-throughput assay system. The extracts identified as autophagy activators were administered to mice with 2% dextran sodium sulfate (DSS). Among the autophagy inducers, Sanguisorba officinalis L. (SO) suppressed DSS-induced colitis. To identify the mechanism by which SO ameliorates colitis, epithelial cell and innate myeloid cells-specific Atg7-deficient mice (Villin-cre; Atg7(f/f) and LysM-cre; Atg7(f/f) mice, respectively) were analyzed. SO-mediated inhibition of colitis was observed in Villin-cre; Atg7(f/f) mice. However, SO and a mixture of its components including catechin acid, ellagic acid, gallic acid, and ziyuglycoside II (Mix4) did not suppressed colitis in LysM-cre; Atg7(f/f) mice. In large intestinal macrophages (Mphi) of Atg7(f/f) mice, SO and Mix4 upregulated the expression of marker genes of anti-inflammatory Mphi including Arg1, Cd206, and Relma. However, these alterations were not induced in LysM-cre; Atg7(f/f) mice. These findings indicate that SO and its active components ameliorate DSS-induced colitis by providing intestinal Mphi with anti-inflammatory profiles via promotion of Atg7-dependent autophagy. |
