<i>Lactobacillus plantarum</i> 69-2 Combined with Galacto-Oligosaccharides Alleviates <scp>d</scp>-Galactose-Induced Aging by Regulating the AMPK/SIRT1 Signaling Pathway and Gut Microbiota in Mice

Wang, Wan; Liu, Fei; Xu, Cong; Liu, Zhijing; Ma, Jiage; Gu, Liya; Jiang, Zhanmei

doi:10.1021/acs.jafc.0c06730

Cited by 46 publications

(42 citation statements)

References 50 publications

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“…Therefore, it is necessary to clarify the mechanism of SIRTs in HCC. The above research results all demonstrate the mechanism by which SIRT1 participates in the body, and it may be possible to make a breakthrough in the treatment of HCC in the future [116]. Additionally, many studies have provided insight into the effects of the clustered regularly spaced short palindrome repeats/CRISPR-associated protein 9 system (CRISPR/Cas9) on SIRT biology, and SIRT editing has shown its relevance to tumors in the latest research.…”

Section: Conclusion and Prospectivementioning

confidence: 75%

Epigenetics of Sirtuins: Relevance to Hepatocellular Carcinoma

Zhu¹,

Wang²,

Chang³

et al. 2021

Oncologie

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Section: Conclusion and Prospectivementioning

confidence: 75%

Epigenetics of Sirtuins: Relevance to Hepatocellular Carcinoma

Zhu¹,

Wang²,

Chang³

et al. 2021

Oncologie

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“…Studies indicate that probiotics can rebuild the intestinal microbial community, increase the colonization of probiotics such as Lactobacillus in the intestinal tract, and protect and improve the integrity of the intestinal barrier [41,42]. Wan found that L. plantarum 69-2 and GOS could activate the hepatic AMPK/SIRT1 signaling pathway by regulating the gut microbiota and metabolites through the liver-gut axis to restore hepatic antioxidant activity in order to alleviate aging [43]. Probiotics regulate the growth of bacteria in the intestinal tract and combine with intestinal toxic molecules to reduce the level of bacterial urea retention in molecules [44].…”

Section: Discussionmentioning

confidence: 99%

Serum Untargeted Metabolism Reveals the Mechanism of L. plantarum ZDY2013 in Alleviating Kidney Injury Induced by High-Salt Diet

et al. 2021

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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.

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“…GOS regulates the gut microbiota and its metabolites through the liver-gut axis. GOS fermentation significantly increases butyrate acid levels, which can activate the hepatic adenosine 5'-monophosphate (AMP)-activated protein kinase (AMPK)/SIRT1 signaling pathway, increase SIRT1 expression, restore hepatic antioxidant activity, and alleviate aging [ 94 ]. However, there is no direct evidence that acarbose affects the SIRT6 longevity gene.…”

Section: Putative Gut Microbiota-mediated Mechanisms For the Extensio...mentioning

confidence: 99%

Extension of the Life Span by Acarbose: Is It Mediated by the Gut Microbiota?

Wu¹,

Yan²,

Yang³

et al. 2022

Aging and disease

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Acarbose can extend the life span of mice through a process involving the gut microbiota. Several factors affect the life span, including mitochondrial function, cellular senescence, telomere length, immune function, and expression of longevity-related genes. In this review, the effects of acarbose-regulated gut microbiota on the life span-influencing factors have been discussed. In addition, a novel theoretical basis for improving our understanding of the mechanisms by which acarbose extends the life span of mice has been suggested.

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Lactobacillus plantarum 69-2 Combined with Galacto-Oligosaccharides Alleviates d-Galactose-Induced Aging by Regulating the AMPK/SIRT1 Signaling Pathway and Gut Microbiota in Mice

Cited by 46 publications

References 50 publications

Epigenetics of Sirtuins: Relevance to Hepatocellular Carcinoma

Epigenetics of Sirtuins: Relevance to Hepatocellular Carcinoma

Serum Untargeted Metabolism Reveals the Mechanism of L. plantarum ZDY2013 in Alleviating Kidney Injury Induced by High-Salt Diet

Extension of the Life Span by Acarbose: Is It Mediated by the Gut Microbiota?

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