恒古骨伤愈合剂对db/db小鼠的降血糖和改善肠道菌群作用研究
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1.云南省执业药师注册中心;2.昆明医科大学;3.云南省第一人民医院

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Effect of Osteoking on lowering blood sugar and improving intestinal flora in db/db mice
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1.Registration Center of Licensed Pharmacists of Yunnan Province;2.kunming medical university;3.First People's Hospital of Yunnan Province

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    摘要:

    目的 探索恒古骨伤愈合剂对db/db小鼠血糖和肠道微生物的影响。方法 将野生小鼠作为对照组,db/db小鼠随机分为模型组和恒古骨伤愈合剂治疗组;灌胃给药12周后,检测空腹血糖,血清糖化血红蛋白和胰岛素含量,使用16S rDNA技术分析小鼠肠内容物菌群变化及预测菌群功能。结果 与模型组比较,恒古骨伤愈合剂降低db/db小鼠空腹血糖(P < 0.01)、血清糖化血红蛋白(P < 0.01)、胰岛素抵抗指数(P < 0.01),升高胰岛素含量(P < 0.01);恒古骨伤愈合剂增加db/db小鼠盲结肠有益菌丰度,降低害菌丰度,其中马文氏菌属的丰度显著升高(P < 0.01);恒古骨伤愈合剂抑制了db/db小鼠菌群D-精氨酸和D-鸟氨酸代谢、鞘脂代谢、半乳糖代谢的降低及赖氨酸降解、硫中继系统、丙酸代谢的升高(P < 0.05)。结论 恒古骨伤愈合剂具有降血糖功效和调节db/db小鼠肠道微生态平衡的作用。

    Abstract:

    Objective:To investigate the effects of Osteoking on hyperglycemia and regulating gut microbiota in db/db mice. Methods:The wild mice were used as the cntrol group and db/db mice were randomly into model group and Osteoking group. After intragastric administration for 12 weeks, Fasting blood glucose, serum glycosylated hemoglobin and insulin levels were measured , the changes of intestinal microflora were determined and functional pathways related to intestinal microflora in mice were predicted by 16S rDNA sequencing technology. Results:Compared with model group, Osteoking decreased fasting blood glucose (P < 0.01), serum glycosylated hemoglobin (P < 0.01), insulin resistance index (P < 0.01), and increased insulin content (P < 0.01) in db/db mice. Osteoking increased the abundance of beneficial bacteria of intestinal microflora, while decreased the abundance of harmful bacteria; the abundance of Marvinbryantia was increased. Osteoking alleviated the decrease of metabolism of D-arginine and D-ornithine, sphingolipid and galactose metabolism( P < 0.05), while inhibited lysine degradation, sulfur relay system and propanoate metabolism( P < 0.05). Conclusion:Osteoking has the effects of hypoglycemic properties and improving the intestinal microflora imbalance in db/db mice.

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  • 收稿日期:2023-02-10
  • 最后修改日期:2023-06-04
  • 录用日期:2023-12-04
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