Objective:To investigate gut microbiota participating in the progression of atherosclerosis through regulatory T cell(Treg)/indoleamine 2,3-dioxygenase-1(IDO1)axis signaling pathway.Methods:Five-week female apolipoprotein E gene knockout(ApoE)mice of C57BL specific pathogen free(SPF)were randomly divided into ordinary feed treatment group(NC group)and high-fat diet(0.2％cholesterol,42％fat)treatment group(HF group),with 10 mice in each group.Aortic plaques and lesions were detected by oil red O staining and hematoxylin-eosin staining.The percentage of CD4+CD25+Foxp3+Treg in spleen cells was detected by flow cytometry.Indoleamine 2,3-dioxygenase(IDO)was quantified by protein immunoblotting,and fecal microbiota was detected by polymerase chain reaction(PCR).Results:Compared with the NC group,the aortic plaque and hardened lesion area in the HF group increased(P＜0.001),and the CD4+CD25+Foxp3+/CD4+T ratio and Foxp3 mRNA level decreased(P＜0.001).Compared with the NC group,the content of IDO1 in the HF group decreased(t=4.98,P＜0.001).The plaques in mice were negatively correlated with Treg and IDO1(r values were-0.87 and-0.66,respectively,P＜0.01).Firmicutes were positively correlated with atherosclerotic plaque(r=0.64,P＜0.01).Actinomycetes were negatively correlated with atherosclerotic plaque(r=-0.74,P＜0.01).Firmicutes were negatively correlated with IDO1(r=-0.59,P＜0.05).Bacteroidetes were positively correlated with IDO1(r=0.67,P＜0.01).Firmicutes were negatively correlated with Treg(r=-0.63,P＜0.01).Proteobacteria were positively correlated with Treg(r=0.61,P＜0.01).Conclusion:The changes of gut microbiota might participate in the progression of high-fat diet atherosclerosis via Treg/IDO1 signaling pathway.
关键词
动脉粥样硬化/肠道菌群/调节性T细胞/吲哚胺2,3-双加氧酶-1/高脂饮食/小鼠/实验研究
Key words
atherosclerosis/gut microbiota/regulatory T cell/indoleamine 2,3-dioxygenase-1/high-fat diet/mice/experimental study
维普
万方数据