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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 (Mix 4 ) did not suppressed colitis in  LysM-cre ;  Atg7   f/f   mice. In large intestinal macrophages (Mφ) of  Atg7   f/f   mice, SO and Mix 4  upregulated the expression of marker genes of anti-inflammatory Mφ 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 Mφ with anti-inflammatory profiles via promotion of Atg7-dependent autophagy.

Sanguisorba officinalis L. derived from herbal medicine prevents intestinal inflammation by inducing autophagy in macrophages