炎症性肠病动物模型可通过化学性诱导、免疫学、遗传学等方法获得。
Animal models of inflammatory bowel disease can be induced by chemical, immunology, genetics and other access methods.
结论：大鼠饥饿后早期确有肠黏膜组织结构受损，发生内毒素移位，同时伴有肠黏膜免疫学屏障受损。
CONCLUSION: the structure of intestinal mucosa is damaged in the earlier stage of starvation in rats, accompanied by endotoxin translocation and dysfunction of intestinal mucosal immune barrier.
目的观察桂枝汤对痹证(胶原诱导免疫性关节炎)小鼠肠黏膜免疫学指标的影响。
ObjectiveTo observe the effect of Guizhi Decocti on (GZD) on immunological indexes in intestinal mucosal immune system of mice with Bi syndrome (collagen induced immune arthritis).
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