Objective: To investigate the effect and possible mechanism of Patrinia scabiosifolia extract on intestinal fibrosis in inflammatory bowel disease (IBD) through intestinal flora regulation of β-defensin 2. Methods: Thirty-six male SD rats were selected and randomly divided into six groups: normal control group (Normal), model group (Model), salazosulfapyridine positive control group (SASP), Patrinia scabiosifolia (PS) high (3.2 g·kg ^-1), medium (2.2 g·kg ^-1), and low dose group (1.1 g·kg ^-1), respectively. Except for the normal control group, which was given an equal volume of saline enema, all other groups of rats were given 50% ethanol enema with 2,4,6-trinitrobenzene sulfonic acid (TNBS) to induce the development of intestinal fibrosis in inflammatory bowel disease. The rats were administered by gavage for 7 days continuously from the second day after modeling, and equal volumes of saline were given to the normal control and model groups once daily. The general behavior of the rats was observed. Gram staining was used to detect changes in intestinal fecal flora. HE staining was used to detect histopathological changes in colonic tissue. masson staining was used to observe fibrosis in colonic tissue. Immunohistochemistry was used to detect α-SMA and TGF-β protein expression in colon tissue. ELISA was used to detect β-defensin 2 and IL-13 expression in colon tissue. Results: Compared with the normal control group, the model group rats showed severe colonic pathological damage and increased blue staining of collagen fibers, suggesting a successful intestinal fibrosis model. Compared with the model group, the PS group administration group could significantly improve the pathological injury and fibrosis degree of IBD intestinal fibrosis rats, down-regulate the abnormally high expression of α-SMA, TGF-β protein (P<0.05), reduce the expression level of β-defensin 2, elevate IL-13 expression levels (P<0.05), and improve the intestinal flora disorder phenomenon. Conclusion: Patrinia scabiosifolia may alleviate the disease process of intestinal fibrosis in IBD by reducing β-defensin 2 expression through modulation of intestinal flora.