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标题：Serum Untargeted Metabolism Reveals the Mechanism of L. plantarum ZDY2013 in Alleviating Kidney Injury Induced by High-Salt Diet
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作者：Cuixiang Wan ; Shufang Chen ; Kui Zhao 等
期刊名称：Nutrients
电子版ISSN：2072-6643
出版年度：2021
卷号：13
期号：11
DOI：10.3390/nu13113920
语种：English
出版社：MDPI Publishing
摘要：A high-salt diet (HSD) is one of the key risk factors for hypertension and kidney injury. In this study, a HSD C57BL/6J mice model was established with 4% NaCl, and then different concentrations of Lactobacillus plantarum ZDY2013 were intragastrically administered for 2 weeks to alleviate HSD-induced renal injury. For the study, 16S rRNA gene sequencing, non-targeted metabonomics, real-time fluorescent quantitative PCR, and Masson’s staining were used to investigate the mechanism of L. plantarum ZDY2013 in alleviating renal damage. Results showed that HSD caused intestinal inflammation and changed the intestinal permeability of mice, disrupted the balance of intestinal flora, and increased toxic metabolites (tetrahydrocorticosteron (THB), 3-methyhistidine (3-MH), creatinine, urea, and L-kynurenine), resulting in serious kidney damage. Interestingly, L. plantarum ZDY2013 contributed to reconstructing the intestinal flora of mice by increasing the level of Lactobacillus and Bifidobacterium and decreasing that of Prevotella and Bacteroides. Moreover, the reconstructed intestinal microbiota significantly changed the concentration of the metabolites of hosts through metabolic pathways, including TCA cycle, ABC transport, purine metabolism, and histidine metabolism. The content of uremic toxins such as L-kynurenine, creatinine, and urea in the serum of mice was found to be decreased by L. plantarum ZDY2013, which resulted in renal injury alleviation. Our data suggest that L. plantarum ZDY2013 can indeed improve chronic kidney injury by regulating intestinal flora, strengthening the intestinal barrier, limiting inflammatory response, and reducing uremic toxins.
关键词：high-salt diets; intestinal flora; kidney injury; Lactobacillus; untargeted metabolism