摘要
目的:探究骨碎补总黄酮对骨关节炎(OA)模型大鼠肠道菌群的影响,并分析其治疗OA的潜在机制。方法:通过Hulth法建立OA大鼠模型,使用骨碎补总黄酮干预后获取大鼠粪便及膝关节软骨。将大鼠膝关节软骨进行病理学观察并进行Mankin's评分以评估模型的建立及骨碎补总黄酮的干预效果。通过16SrDNA基因测序技术检测各组大鼠肠道菌群的变化。结果:骨碎补总黄酮进行干预后,OA大鼠软骨退变得到改善,Mankin’s评分降低(P<0.05)。LEfSe分析显示经骨碎补总黄酮治疗后,罗姆布茨菌属、瘤胃球菌属、消化链球菌科、鼠乳杆菌种等相对丰度下降,Muri菌科相对丰度显著升高。KEGG富集结果表明,相关肠道菌落调控OA与碳水化合物代谢、糖合成代谢和能量代谢密切相关。结论:骨碎补总黄酮可能通过促进肠道内有益菌生长,抑制有害菌繁殖调整大鼠肠道内微生态平衡,减轻肠道内炎症反应,发挥OA的治疗作用。
Objective:To explore effects of total flavonoids of Drynariae Rhizoma on intestinal flora of osteoarthritis rats,and to analyze the potential mechanisms of treatment of osteoarthritis.Methods:The OA model was established by Hulth's method.After the intervention group was given total flavonoids of Drynariae Rhizoma,obtained cartilages of rat knee joint were subjected to pathological observations and Mankin's score for the purpose of evaluation of the establishment of the model and the intervention effect of total flavonoids of Drynariae Rhizoma.Changes of intestinal flora of the rats were detected by 16S rDNA sequencing technology analysis.Results:After the intervention with total flavonoids of Drynariae Rhizoma,degeneration of knee joint cartilages from OA rats were ameliorated,and Mankin's score declined(P<0.05).LEfSe analysis showed that Romboutsia,Ruminococcus,Peptostreptococcaceae,Lactobacillus murinus,Lactobacillus murinus,etc declined in relative abundances,but Muribaculaceae increased in relative abundances after the treatment of total flavonoids of Drynariae Rhizoma.KEGG pathway enrichment analysis demonstrated that intestinal colonies which regulated OA were closely associated with Carbohydrate Metabolism,Energy Metabolism and Glycan Biosynthesis and Metabolism.Conclusion:Total flavonoids of Drynariae Rhizoma can improve the intestinal microecological balance and attenuate gut inflammatory responses of OA rats in that it can promote the growth of beneficial microbes and inhibit the pullulation of harmful microbes.
作者
陈光耀
佟常青
曲润敏
余新波
罗静
王金平
陶庆文
CHEN Guang-yao;TONG Chang-qing;QU Run-min;YU Xin-bo;LUO Jing;WANG Jin-ping;TAO Qing-wen(Beijing University of Chinese Medicine,Beijing 100029,China;Department of TCM Rheumatology,China-Japan Friendship Hospital,Beijing 100029,China;Beijing Key Lab for Immune-Mediated Inflammatory Diseases,Beijing 100029,China)
出处
《中华中医药杂志》
CAS
CSCD
北大核心
2022年第12期7321-7327,共7页
China Journal of Traditional Chinese Medicine and Pharmacy
基金
国家自然科学基金面上项目(No.81673941)
国家临床重点专科能力建设项目(No.2011-ZDZK-001)