Tributyrin alleviates gut microbiota dysbiosis to repair intestinal damage in antibiotic-treated mice.
Tributyrin alleviates gut microbiota dysbiosis to repair intestinal damage in antibiotic-treated mice.
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DOI：
10.1371/journal.pone.0289364
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发表时间：
2023
期刊：
影响因子：
3.7
通讯作者：
中科院分区：
文献类型：
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作者：
三丁酸甘油酯（TB）是丁酸前体，通过缓慢释放丁酸在抗炎和肠屏障修复作用中具有关键作用。然而，它在抗生素引起的肠道微生物群失调中的作用仍不清楚。在此，我们建立了一个肠道菌群失调模型，通过灌胃头孢曲松钠，以研究不同剂量的TB对恢复肠道菌群和肠道损伤的影响。首先，将C57 BL/6雄性小鼠分为对照组（NC，n = 8）和实验组（ABx，n = 24），分别灌胃生理盐水0.2mL和头孢曲松钠400 mg/mL溶液7 d（2次/d，中间间隔6 h）。然后，将ABx组小鼠随机分为模型组（M，0.2mL生理盐水）、低TB组（TL，0.3g/kg BW）和高TB组（TH，3g/kg BW），共11 d。我们发现，结核病补充剂减轻了疟疾引起的体重减轻、腹泻和肠道组织损伤。16 S rRNA序列分析显示，与M组相比，TB干预增加了肠道植物群的α多样性，增加了潜在的短链脂肪酸（SCFA）产生菌（如Muribaculaceae和双歧杆菌），并抑制了潜在致病菌（如拟杆菌属和肠球菌属）的相对丰度。TB补充剂逆转了经抗结核治疗的小鼠中SCFAs产生的减少。此外，TB还下调了血清LPS和zonulin、肠组织中TNF-α、IL-6、IL-1β和NLRP 3炎性相关因子的水平，上调了紧密连接蛋白（如ZO-1和Occludin）和MUC 2的水平。总体而言，低剂量TB对上述指标的调节能力强于高剂量TB。总之，TB可以恢复肠道微生物群的生态失调，增加SCFAs，抑制炎症，并改善禁食诱导的肠道损伤，表明TB可能是一种潜在的肠道微生物群调节剂。
Tributyrin (TB) is a butyric acid precursor and has a key role in anti-inflammatory and intestinal barrier repair effects by slowly releasing butyric acid. However, its roles in gut microbiota disorder caused by antibiotics remain unclear. Herein, we established an intestinal microbiota disorder model using ceftriaxone sodium via gavage to investigate the effects of different TB doses for restoring gut microbiota and intestinal injury. First, we divided C57BL/6 male mice into two groups: control (NC, n = 8) and experimental (ABx, n = 24) groups, receiving gavage with 0.2 mL normal saline and 400 mg/mL ceftriaxone sodium solution for 7 d (twice a day and the intermediate interval was 6 h), respectively. Then, mice in the ABx group were randomly split into three groups: model (M, 0.2 mL normal saline), low TB group (TL, 0.3 g/kg BW), and high TB group (TH, 3 g/kg BW) for 11 d. We found that TB supplementation alleviated antibiotics-induced weight loss, diarrhea, and intestinal tissue damage. The 16S rRNA sequence analysis showed that TB intervention increased the α diversity of intestinal flora, increased potential short-chain fatty acids (SCFAs)-producing bacteria (such as Muribaculaceae and Bifidobacterium), and inhibited the relative abundance of potentially pathogenic bacteria (such as Bacteroidetes and Enterococcus) compared to the M group. TB supplementation reversed the reduction in SCFAs production in antibiotic-treated mice. Additionally, TB downregulated the levels of serum LPS and zonulin, TNF-α, IL-6, IL-1β and NLRP3 inflammasome-related factors in intestinal tissue and upregulated tight junction proteins (such as ZO-1 and Occludin) and MUC2. Overall, the adjustment ability of low-dose TB to the above indexes was stronger than high-dose TB. In conclusion, TB can restore the dysbiosis of gut microbiota, increase SCFAs, suppress inflammation, and ameliorate antibiotic-induced intestinal damage, indicating that TB might be a potential gut microbiota modulator.
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影响因子：
16.6
作者：
Duvallet C;Gibbons SM;Gurry T;Irizarry RA;Alm EJ
通讯作者：
Alm EJ
影响因子：
24.1
作者：
Akbal, Anil;Dernst, Alesja;Lovotti, Marta;Mangan, Matthew S. J.;McManus, Roisin M.;Latz, Eicke
通讯作者：
Latz, Eicke
DOI：
10.1016/j.aninu.2022.06.004
发表时间：
2022-09
期刊：
Animal nutrition (Zhongguo xu mu shou yi xue hui)
影响因子：
--
作者：
通讯作者：
--
影响因子：
24.5
作者：
Bauer, Christian;Duewell, Peter;Schnurr, Max
通讯作者：
Schnurr, Max
DOI：
10.1097/mpg.0000000000000369
发表时间：
2014-08-01
影响因子：
2.9
作者：
Huang, Xiao-Zhong;Li, Zhong-Rong;Lin, Jing
通讯作者：
Lin, Jing