Gao Ruijuan, Wang Chunjie, Han Aricha, Tian Yanping, Ren Shunan, Lv Wenting, Chen Aorigele, Zhang Jian
College of Veterinary Medicine, Inner Mongolia Agricultural University, Hohhot 010018, China.
College of Animal Science, Inner Mongolia Agricultural University, Hohhot 010018, China.
Animals (Basel). 2021 Nov 19;11(11):3314. doi: 10.3390/ani11113314.
The effect of emodin on the intestinal mucosal barrier of a mouse O-induced diarrhea model was observed. Following successful establishment of a diarrhea model, the mice were treated with drugs for seven days. Intestinal lesions and the shape and the number of goblet cells were assessed via hematoxylin-eosin and periodic-acid-Schiff staining, while changes in inflammatory factors, ultrastructure of the small intestine, expression of MUC-2, and changes in the intestinal microbiota were analyzed via RT-PCR, electron microscopy, immunofluorescence, and 16S rRNA sequencing. Examination showed that emodin ameliorated pathological damage to the intestines of diarrheic mice. RT-PCR indicated that emodin reduced TNF-α, IL-β, IL-6, MPO, and COX-2 mRNA levels in duodenal tissues and increased the levels of sIgA and MUC-2 and the number of goblet cells. Microbiome analysis revealed that O reduced bacterial richness and altered the distribution pattern of bacterial communities at the phylum and order levels in cecum contents. Notably, pathogenic and were significantly increased in diarrheic mice. However, emodin reversed the trend. Thus, emodin protected against intestinal damage induced by O and improved intestinal mucosal barrier function in mice by increasing the abundance of beneficial intestinal microbiota and inhibiting the abundance of harmful bacteria, thereby alleviating diarrhea.
观察了大黄素对小鼠O诱导腹泻模型肠道黏膜屏障的影响。腹泻模型成功建立后,用药物治疗小鼠7天。通过苏木精-伊红染色和过碘酸-希夫染色评估肠道病变以及杯状细胞的形态和数量,同时通过逆转录-聚合酶链反应(RT-PCR)、电子显微镜、免疫荧光和16S核糖体RNA测序分析炎症因子的变化、小肠超微结构、黏蛋白2(MUC-2)的表达以及肠道微生物群的变化。检查显示大黄素改善了腹泻小鼠肠道的病理损伤。RT-PCR表明大黄素降低了十二指肠组织中肿瘤坏死因子-α(TNF-α)、白细胞介素-β(IL-β)、白细胞介素-6(IL-6)、髓过氧化物酶(MPO)和环氧化酶-2(COX-2)的信使核糖核酸(mRNA)水平,并提高了分泌型免疫球蛋白A(sIgA)和MUC-2的水平以及杯状细胞的数量。微生物组分析显示,O降低了细菌丰富度,并改变了盲肠内容物在门和纲水平上的细菌群落分布模式。值得注意的是,腹泻小鼠中致病性和显著增加。然而,大黄素逆转了这一趋势。因此,大黄素可预防O诱导的肠道损伤,并通过增加有益肠道微生物群的丰度和抑制有害细菌的丰度来改善小鼠肠道黏膜屏障功能,从而减轻腹泻。