ReferenceID 920
Carotenoid Extract Derived from Euglena gracilis Overcomes Lipopolysaccharide-Induced Neuroinflammation in Microglia: Role of NF-κB and Nrf2 Signaling Pathways
Mol Neurobiol
Activation of microglia results in the increased production and release of a series of inflammatory and neurotoxic mediators, which play essential roles in structural and functional neuronal damage and in the development
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- Reference Id
- 920
- Evidence Id
- 17510
- Core Evidence Id
- 17510
- Source Reference Id
- 1827
- Herb2 Reference Id
- HBREF002624
- Subject Paper Key
- HERB005893_33745115
- Pubmed Id
- 33745115
- Doi
- 10.1007/s12035-021-02353-6
- Paper Title
- Carotenoid Extract Derived from Euglena gracilis Overcomes Lipopolysaccharide-Induced Neuroinflammation in Microglia: Role of NF-κB and Nrf2 Signaling Pathways
- Paper Abstract
- Activation of microglia results in the increased production and release of a series of inflammatory and neurotoxic mediators, which play essential roles in structural and functional neuronal damage and in the development and progression of a number of neurodegenerative diseases. The microalga Euglena gracilis (Euglena), rich in vitamins, minerals, and other nutrients, has gained increasing attention due to its antimicrobial, anti-viral, antitumor, and anti-inflammatory activities. In particular, anti-inflammatory properties of Euglena could exert neuroprotective functions in different neurodegenerative diseases related to inflammation. However, the mechanisms underlying the anti-inflammatory effect of Euglena are not fully understood. In this study, we investigated whether Euglena could attenuate microglia activation and we also studied the mechanism of its anti-inflammatory activity. Our results showed that non-cytotoxic concentrations of a Euglena acetone extract (EAE) downregulated the mRNA expression levels and release of pro-inflammatory mediators, including NO, IL-1beta, and TNF-alpha in LPS-stimulated microglia. EAE also significantly blocked the LPS-induced nuclear translocation of NF-kappaB p65 subunit and increased the mRNA expression of nuclear factor erythroid 2-related factor (Nrf2) and heme oxygenase-1 (HO-1). Furthermore, the release of pro-inflammatory mediators and NF-kappaB activation were also blocked by EAE in the presence of ML385, a specific Nrf2 inhibitor. Together, these results show that EAE overcomes LPS-induced microglia pro-inflammatory responses through downregulation of NF-kappaB and activation of Nrf2 signaling pathways, although the two pathways seem to get involved in an independent manner.
- Journal
- Mol Neurobiol
- Publish Year
- 2021
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Neurodegenerative Diseases; Inflammation
- Paper Title Cn
- Paper Title En
- Carotenoid Extract Derived from Euglena gracilis Overcomes Lipopolysaccharide-Induced Neuroinflammation in Microglia: Role of NF-κB and Nrf2 Signaling Pathways
- Bilingual Status
- semi_complete