关键词: 小肠结肠炎, Nod信号接头蛋白质类, 细胞焦亡, 小鼠, 近交BALB C, 肠黏膜细胞

Abstract: Objective To investigate the expression level of NLRP3 in intestinal mucosal cells of mouse model with food protein-induced enterocolitis syndrome (FPIES), and to clarify the relationship between inflammatory molecules and cell pyroptosis induced by abnormal expression of NLRP3. Methods The FPIES mouse model was established by ovalbumin intragastric administration. Fluorescent quantitative PCR and Western blot methods were used to detect the expression levels of NLRP3, inflammatory molecules and pyrolytic pathway molecules. Western blot assay was used to detect the expression levels of inflammatory molecules and pyrolytic pathway molecules in intestinal mucosal cells after activating or inhibiting NLRP3. Results The expression levels of NLRP3, inflammatory molecules and pyrolytic pathway molecules in intestinal mucosal cells were significantly up-regulated in FPIES model mice (P＜0.05). The activation of NLRP3 expression could significantly up-regulate the expression of inflammatory molecules and pyrolytic pathway molecules, and the inhibition of NLRP3 expression could significantly up-regulate the expression of TGF- β and TNF- α (P＜0.05). Conclusion The expression of NLRP3 in intestinal mucosal cells is closely related to the inflammatory response and cell pyroptosis in FPIES model mice, which is the upstream target molecule to regulate FPIES intestinal pathological phenotypes.

Key words: enterocolitis, Nod signaling adaptor proteins, pyroptosis, mice, inbred BALB C, intestinal mucosa cell