低聚果糖通过调整肠道菌群改善川崎病小鼠冠状动脉损伤的机制

目的：探讨低聚果糖（FOS）通过调整肠道菌群改善川崎病（KD）小鼠冠状动脉损伤的内在机制。方法：采用白色念珠菌细胞壁水溶性成分（CAWS）建立KD模型，随机分为正常对照（PBS）组，KD造模（CAWS）组，FOS+KD（FOS）组，28 d造模成功后，收集粪便和心脏。通过HE染色和免疫荧光检测冠状动脉的结构变化和单核巨噬细胞的浸润程度。利用16S rRNA测序和气相色谱与质谱联用（GS-MS）技术，分析各组肠道菌群和代谢产物短链脂肪酸（SCFAs）的差异。结果：HE染色结果表明KD造模后多处冠状动脉正常结构消失，管壁水肿，炎症细胞大量浸润。免疫荧光显示CD68单核巨噬细胞标记物在冠脉周围显著增强。经过FOS处理后，上述的冠状动脉损伤及炎症情况显著下降。16S rRNA测序发现CAWS组肠道菌群明显紊乱，产SCFAs菌群减少，粪便SCFAs含量下降，FOS处理后肠道菌群组成情况及SCFAs有所恢复。结论：FOS能改善KD小鼠的肠道菌群紊乱，提高SCFAs产量，减轻KD冠状动脉损伤。

The mechanism of fructo-oligosaccharides in the attenuation of coronary artery injury in mice with Kawasaki disease by regulating intestinal flora

Objective: To investigate the underlying mechanism for fructo-oligosaccharide to attenuate coronary artery injury in mice with Kawasaki disease (KD) by regulating intestinal flora. Methods: Mice were given water-soluble components of Candida albicans cell wall (CAWS) to establish KD model and randomly assigned as normal control group (PBS), KD model group (CAWS), and FOS+KD group (FOS). After 28 days of modeling, feces and hearts were collected. The structural changes of coronary arteries and the infiltration degree of monocyte-macrophages were detected by HE and immunofluorescence with CD68 antibody, respectively. The differences in intestinal flora and metabolites of short-chain fatty acids (SCFAs) were analyzed by 16S rRNA sequencing and gas chromatography/mass spectrometry (GS-MS). Results: HE results showed that after KD modeling, many normal structures of coronary arteries disappeared. Wall edema and a large number of inflammatory cells were infiltrated. Immunofluorescence showed significant enhancement of CD68, the monocyte-macrophage markers, around coronary arteries. After FOS treatment, the above coronary artery injury and inflammation decreased significantly. 16S rRNA sequencing showed that intestinal flora in CAWS group was obviously disturbed, SCFAs producing flora and fecal SCFAs content decreased. However, intestinal flora composition and SCFAs recovered after FOS treatment. Conclusion: FOS alleviated coronary artery injury of KD mice through regulating intestinal flora disturbance to increase SCFAs production