Jiangsu Vocational College of Medicine, Yancheng 224005, China.
Gaoyou Pelple's Hospital, Yangzhou 225600, China.
Molecules. 2022 Oct 29;27(21):7357. doi: 10.3390/molecules27217357.
Dysbiosis is a crucial manifestation of dyslipidemia; however, oral supplementation of probiotic modulates the intestinal commensal composition. The protective mechanism of probiotics against hyperlipidemia is still under investigation. To elucidate the hypolipidemic effect of TR08 through the analysis of gut microbiota and lipid metabolomics, we investigated changes in gut microbiota and lipid metabolomic phenotypes in mice by real time quantitative PCR and untargeted metabolomics analysis. High fat diet-induced dyslipidemia mice were orally administered with TR08 for 8 weeks. The proinflammatory cytokines (interleukin-2 and interferon-γ) levels in spleen and aortic wall injury in the mice fed with a high-fat diet were inhibited after treatment with TR08 at 1 × 10 CFU per day per mouse. TR08 also reshaped the gut microbiota with increases of the relative abundances of Bifidobacterium and Bacteroides, reduced the abundance of the pro-pathogen bacterial Enterococcus, increased the serum level of short chain fatty acids (SCFAs) contents, and promoted sphingomholipid metabolic pathway. The results indicated that TR08 could improve the intestinal microbiota of mice to increase the production of SCFAs, and then play the anti-inflammation induced by hyperlipidemia and reduce the inflammatory injury of blood vessel wall. Therefore, TR08 can potentially be used as a hypolipidemic effect probiotic in further interventions.
肠道菌群失调是血脂异常的重要表现；然而，益生菌的口服补充可以调节肠道共生组成。益生菌防治高血脂的保护机制仍在研究中。为了通过分析肠道微生物群和脂质代谢组学来阐明 TR08 的降血脂作用，我们通过实时定量 PCR 和非靶向代谢组学分析研究了高脂饮食诱导的血脂异常小鼠肠道微生物群和脂质代谢表型的变化。用 TR08 对高脂饮食喂养的小鼠进行 8 周的口服治疗，可抑制高脂饮食喂养小鼠脾脏和主动脉壁损伤中的促炎细胞因子（白细胞介素 2 和干扰素-γ）水平。TR08 还重塑了肠道微生物群，双歧杆菌和拟杆菌的相对丰度增加，病原菌肠球菌的丰度降低，血清短链脂肪酸（SCFA）含量增加，并促进鞘脂代谢途径。结果表明，TR08 可以改善小鼠的肠道微生物群，增加 SCFA 的产生，从而发挥抗高血脂诱导的炎症作用，并减轻血管壁的炎症损伤。因此，TR08 可能在进一步的干预中用作具有降血脂作用的益生菌。
