Abstract: Taking the model organism zebrafish (Danio Rerio) as the research object, the toxic effects and molecular mechanism of chronic exposure of decabromodiphenyl ether (BDE-209) on intestinal tissue were explored. Zebrafish were exposed to different concentrations of BDE-209 (6, 60, and 600 μg/L, dimethyl sulfoxide solvent control) for 28 d. The intestinal tissue of zebrafish was pathologically examined by hematoxylin-eosin (H & E) staining. The contents of biomarkers related to oxidative stress and inflammatory response in the intestine were analyzed by biochemical indicators and ELISA experiments. The relative expression of genes related to the intestinal barrier, inflammatory response, and apoptosis was analyzed by real-time qPCR. The results showed that BDE-209 exposure resulted in thinning of the intestinal wall, increase of vacuolation in intestinal villi and external longitudinal muscle, damage of intestinal wall and cilia, and down-regulation of intestinal ZO-1, Claudin-2, and Tjp2a mRNA relative expression to affect intestinal physical barrier function. BDE-209 exposure increased the contents of reactive oxygen species (ROS), malondialdehyde (MDA), catalase (CAT), and superoxide dismutase (SOD) in the intestine, indicating that BDE-209 exposure caused intestinal oxidative stress. In addition, BDE-209 exposure up-regulated the contents of pro-inflammatory cytokines tumor necrosis factor α (TNF-α) and interleukin 1β (IL-1β) and the content of lipopolysaccharide (LPS) in the intestine, leading to increased intestinal inflammatory response, and increased the expression of p53, Bax, Caspase3 gene and down-regulated Bcl2 gene expression, promoting the apoptosis of zebrafish intestine.