吲哚-3-丙酸通过C/EBP同源蛋白基因介导的凋亡通路缓解猪δ冠状病毒感染诱导的肠上皮损伤OA
Indole-3-propionic acid alleviates porcine deltacoronavirus-induced intestinal epithelial injury via C/EBP homologous protein gene-mediated apoptotic pathway
猪δ冠状病毒(porcine deltacoronavirus,PDCoV)感染可导致仔猪严重肠炎,并引发高死亡率.本研究通过系统筛选具有缓解PDCoV感染相关内质网应激潜力的吲哚类代谢物,并对其作用机制进行了探究.结果显示,PDCoV感染可诱导肠上皮内质网应激与细胞凋亡.在多种吲哚类化合物中,吲哚-3-丙酸表现出显著的内质网应激抑制功能,并同步降低细胞凋亡水平.在猪小肠类器官及小鼠感染模型中进一步证实吲哚-3-丙酸可特异性抑制十二指肠上皮细胞的内质网应激及其介导的细胞凋亡.综上所述,本研究表明吲哚-3-丙酸能够通过调控内质网应激通路减轻PDCoV感染所致的肠上皮损伤,为开发以菌群代谢物为基础的抗肠道冠状病毒营养干预策略提供了新的理论依据与数据支撑.
Porcine deltacoronavirus(PDCoV)infection can cause severe enteritis in piglets,leading to high mortality rates.This study systematically screened indole metabolites with the potential to alleviate PDCoV-associated endoplasmic reticulum stress(ERS)and conducted an investigation into their mechanisms of action.The results showed that PDCoV infection could induce ERS and apoptosis in intestinal epithelial cells.Among various indole compounds,indole-3-propionic acid(IPA)demonstrated a significant inhibitory effect on ERS and concurrently reduced the level of apoptosis.Further validation in porcine small intestinal organoids and mouse infection models confirmed that IPA could specifically inhibit ERS and its mediated apoptosis in duodenal epithelial cells.In conclusion,this study demonstrates that IPA can alleviate PDCoV-induced intestinal epithelial damage by modulating the ERS pathway,providing a new theoretical foundation and empirical support for developing microbiota metabolite-based nutritional intervention strategies against enteric coronaviruses.
华陈钢;屈阳;朱书;冀伟
浙江大学动物科学学院,浙江 杭州 310058中国农业科学院上海兽医研究所,上海 200241浙江大学动物科学学院,浙江 杭州 310058浙江海正动物保健品有限公司,浙江 杭州 311401
农业科技
猪δ冠状病毒吲哚-3-丙酸内质网应激细胞凋亡
porcine deltacoronavirusindole-3-propionic acidendoplasmic reticulum stressapoptosis
《浙江大学学报(农业与生命科学版)》 2026 (4)
585-597,13
江苏省农业科技自主创新资金项目[CX(24)1010].
评论