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Activation of Nrf2 signaling by natural products-can it alleviate diabetes?

ABSTRACT: Type 2 diabetes mellitus (DM) has reached pandemic proportions and effective prevention strategies are wanted. Its onset is accompanied by cellular distress, the nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor boosting cytoprotective responses, and many phytochemicals activate Nrf2 signaling. Thus, Nrf2 activation by natural products could presumably alleviate DM. We summarize function, regulation and exogenous activation of Nrf2, as well as diabetes-linked and Nrf2-susceptible forms of cellular stress. The reported amelioration of insulin resistance, ?-cell dysfunction and diabetic complications by activated Nrf2 as well as the status quo of Nrf2 in precision medicine for DM are reviewed.

SUBMITTER: Matzinger M

PROVIDER: S-EPMC5967606 | biostudies-literature | 2018 Nov

REPOSITORIES: biostudies-literature

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Activation of Nrf2 signaling by natural products-can it alleviate diabetes?

Matzinger Manuel M Fischhuber Katrin K Heiss Elke H EH

Biotechnology advances 20171228 6

Type 2 diabetes mellitus (DM) has reached pandemic proportions and effective prevention strategies are wanted. Its onset is accompanied by cellular distress, the nuclear factor erythroid 2-related factor 2 (Nrf2) is a transcription factor boosting cytoprotective responses, and many phytochemicals activate Nrf2 signaling. Thus, Nrf2 activation by natural products could presumably alleviate DM. We summarize function, regulation and exogenous activation of Nrf2, as well as diabetes-linked and Nrf2- ...[more]

PMID: 29289692

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Project description:Background and aimsHepatic sinusoidal obstruction syndrome (HSOS) is caused by toxic injury, such as pyrrolizidine alkaloids, to the liver sinusoidal endothelial cells, and the gut microbiota may be involved. However, the specific role and underlying mechanism of gut microbiota in HSOS is unknown.MethodsHSOS model was established by gavage of monocrotaline (MCT) in rats. Fecal microbiota transplantation (FMT) with HSOS-derived or healthy gut flora was also conducted to validate the role of gut microflora in MCT-induced liver injury. The microbial 16 s rRNA analysis and untargeted metabolomics analysis in the faeces were performed to identify HSOS-related flora and metabolites. Finally, by supplementation with specific tryptophan metabolites, such as indole-3-acetaldehyde (IAAld) and indole acetic acid (IAA), we further confirmed the role of tryptophan metabolism in HSOS and the role of the AhR/Nrf2 pathway in MCT-induced liver injury.ResultsMCT induced HSOS-like liver injury in rats with significantly altered gut microbiota. Particularly, some tryptophan-metabolizing bacteria reduced in MCT-treated rats, such as Bacteroides, Bifidobacterium, Lactobacillus and Clostridium, and accompanied by a decrease in microbial tryptophan metabolic activity and a series of tryptophan derivatives. Restoring the gut microbiota via FMT improved MCT-induced liver damage, while HSOS-derived gut microbiota aggravated the liver injury induced by MCT. Supplementation with microbial tryptophan derivatives (IAAld or IAA), or 6-formylindolo(3,2-b)carbazole (Ficz, an AhR agonist) could activate the AhR/Nrf2 signaling pathway, thereby attenuating the MCT-induced liver oxidative stress and liver sinusoidal endothelial cells injury.ConclusionsGut microbiota plays a critical role in MCT-induced HSOS, with inadequate microbial tryptophan metabolism in the gut and consequently a lower activity of the AhR/Nrf2 signaling pathway in the liver, which should be a potential target for the management of HSOS.

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Activation of Nrf2 signaling by natural products-can it alleviate diabetes?

Publications

Activation of Nrf2 signaling by natural products-can it alleviate diabetes?

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