食品科学 ›› 2023, Vol. 44 ›› Issue (3): 170-178.doi: 10.7506/spkx1002-6630-20211118-232

• 营养卫生 • 上一篇    下一篇

动物双歧杆菌乳亚种XLTG11对克林霉素诱导的抗生素相关性腹泻的改善作用

马岩,王中江,杨靖瑜,李哲,彭霞,单秀峰,李柏良,马微微   

  1. (1.沈阳师范大学实验教学中心,辽宁?沈阳 110034;2.东北农业大学食品学院,黑龙江?哈尔滨 150000;3.黑龙江中医药大学药学院,黑龙江?哈尔滨 150000)
  • 出版日期:2023-02-15 发布日期:2023-02-28
  • 基金资助:
    辽宁省科技厅重点研发计划项目(2020JH2/10200039);2022教育部产学合作协同育人项目(220505421095029)

Alleviative Effect of Bifidobacterium animalis subsp. lactis XLTG11 on Antibiotic-Associated Diarrhea Induced by Clindamycin

MA Yan, WANG Zhongjiang, YANG Jingyu, LI Zhe, PENG Xia, SHAN Xiufeng, LI Bailiang, MA Weiwei   

  1. (1. Experimental Teaching Center, Shenyang Normal University, Shenyang 110034, China;2. College of Food Science, Northeast Agricultural University, Harbin 150000, China;3. College of Pharmacy, Heilongjiang University of Chinese Medicine, Harbin 150000, China)
  • Online:2023-02-15 Published:2023-02-28

摘要: 目的:通过克林霉素诱导抗生素相关性腹泻(antibiotic-associated diarrhea,AAD)模型,探究动物双歧杆菌乳亚种XLTG11缓解小鼠AAD的作用。方法:将48 只6 周龄C57BL/6N雄鼠随机分为4 组:对照组、模型组、低剂量组和高剂量组,除对照组外,各组小鼠连续14 d灌胃克林霉素(250 mg/(kg mb·d))诱导AAD模型,然后低剂量组和高剂量组灌胃不同剂量(0.2 mL,5×106、1×107 CFU)动物双歧杆菌乳亚种XLTG11,测定小鼠体质量增长量、盲肠质量、粪便含水量和粪便稠度,测定结肠肿瘤坏死因子α、白细胞介素6(interleukin 6,IL-6)、IL-1β、IL-10水平,血清脂多糖(lipopolysaccharide,LPS)和D-乳酸质量浓度,测定肠道菌群组成及短链脂肪酸含量,以及肠道屏障和核因子κB(nuclear factor kappa-B,NF-κB)信号通路相关基因表达水平。结果:高剂量动物双歧杆菌乳亚种XLTG11显著提高AAD模型小鼠的体质量增长量和抗炎细胞因子水平(P<0.05),显著降低盲肠质量、粪便含水量、粪便稠度评分、促炎细胞因子水平、血清LPS和D-乳酸质量浓度(P<0.05),显著上调闭锁小带蛋白1、Occludin、Claudin-1和黏蛋白2基因的表达水平,调节肠道菌群组成,粪便中乙酸、丙酸和丁酸含量显著增加,显著下调Toll样受体4(Toll like receptor 4,TLR4)、髓分化因子88(myeloid differentiation factor 88,MyD88)和NF-κB信号通路相关基因的表达水平。结论:动物双歧杆菌乳亚种XLTG11能够改善AAD模型小鼠腹泻相关指标,调节细胞因子和肠道菌群组成,提高短链脂肪酸含量,提高肠道屏障相关基因的表达和抑制TLR4/MyD88/NF-κB信号通路的激活,进而有效缓解克林霉素诱导的AAD。

关键词: 动物双歧杆菌乳亚种XLTG11;抗生素相关性腹泻;肠道菌群;短链脂肪酸;NF-kB信号通路

Abstract: Objective: To investigate the relieving effect of Bifidobacterium animalis subsp. lactis XLTG11 on antibiotic-associated diarrhea (AAD) in mice using clindamycin-induced AAD model. Methods: Forty-eight 6-week-old C57BL/6N male mice were randomly divided into four groups: normal control, model, low-dose and high-dose XLTG11. All mice except for the control group were administered with clindamycin orally daily for 14 days to induce AAD, The low-dose and high-dose groups were given 0.2 mL of the bacterial suspensions with viable count of 5 × 106 and 1 × 107 CFU, respectively. Body mass gain, cecum mass, fecal water content and fecal consistency score were measured. The levels of tumor necrosis factor α (TNF-α), interleukin 6 (IL-6), IL-1β, and IL-10 in cecum tissue and the serum levels of lipopolysaccharide (LPS) and D-lactic acid were determined. The gut microbiota composition and the fecal contents of short-chain fatty acids were detected. The expression levels of genes related to the intestinal barrier and the nuclear factor kappa-B (NF-kB) pathway were determined. Results: The high dose of Bifidobacterium animalis subsp. lactis XLTG11 significantly increased the body mass gain and anti-inflammatory cytokine levels (P < 0.05), and significantly decreased cecum mass, fecal water content, fecal consistency score and proinflammatory cytokine levels in the mouse model mice of AAD. Moreover, it significantly up-regulated the gene expression levels of ZO-1, occludin, claudin-1 and MUC2, regulated the composition of the gut microbiota, evidently increased the fecal contents of acetate, propanoate, and butanoate, and significantly down-regulated the expression levels of genes related to the Toll like receptor 4 (TLR4), myeloid differentiation factor (MYD88) and NF-κB signaling pathway. Conclusion: Bifidobacterium animalis subsp. lactis XLTG11 can effectively alleviate AAD symptoms in mice by regulating cytokines and the gut microbiota, increasing fecal short-chain fatty acid contents, increasing the expression levels of intestinal barrier related genes and inhibiting the activation of the TLR4/MyD88/NF-kB signaling pathway.

Key words: Bifidobacterium animalis subsp. lactis XLTG11; antibiotic-associated diarrhea; gut microbiota; short-chain fatty acids; nuclear factor κB signaling pathway

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