ReferenceID 5610
Liquiritin protects PC12 cells from corticosterone-induced neurotoxicity via regulation of metabolic disorders, attenuation ERK1/2-NF-κB pathway, activation Nrf2-Keap1 pathway, and inhibition mitochondrial apoptosis pathway
Food Chem Toxicol
Liquiritin, a flavone derived from the medicine food homology plant liquorice, possesses neuroprotective. However, the neuroprotective mechanism is not clear. In this study, metabolomics based LC-MS was performed to disc
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Record Fields
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- Reference Id
- 5610
- Evidence Id
- 22200
- Core Evidence Id
- 22200
- Source Reference Id
- 4441
- Herb2 Reference Id
- HBREF005238
- Subject Paper Key
- HBIN033383_33035630
- Pubmed Id
- 33035630
- Doi
- 10.1016/j.fct.2020.111801
- Paper Title
- Liquiritin protects PC12 cells from corticosterone-induced neurotoxicity via regulation of metabolic disorders, attenuation ERK1/2-NF-κB pathway, activation Nrf2-Keap1 pathway, and inhibition mitochondrial apoptosis pathway
- Paper Abstract
- Liquiritin, a flavone derived from the medicine food homology plant liquorice, possesses neuroprotective. However, the neuroprotective mechanism is not clear. In this study, metabolomics based LC-MS was performed to discover the metabolite changes in PC12 cells treated with corticosterone-induced neurotoxicity after liquiritin treatment. A total of 30 metabolites were identified as differential metabolites. Among them, 11 metabolites were regulated by liquiritin, and involved in the D-glutamine and D-glutamate metabolism, and glutathione metabolism, etc. Based on the results of metabolomics, three cell signaling pathways related to these metabolic pathways were verified. The results showed that the ERK1/2-NF-kappaB pathway related to the D-glutamine and D-glutamate metabolism was attenuated by liquiritin via down-regulation phospho-ERK1/2, phospho-IkappaBalpha, phospho-NF-kappaB protein expression levels. Furthermore, the Nrf2-Keap1 pathway related to glutathione metabolism was activated by liquiritin via up-regulation Nrf2, Keap1, HO-1, NQO1 protein expression levels, and increased SOD, CAT, GSH-PX enzyme activity, thus exerting antioxidant activity. Additionally, liquiritin inhibited the mitochondrial apoptosis by decreasing the Ca2+ concentration, improving MMP, up-regulating Bcl-2, and down-regulating Bax, cytochrome C, cleaved-Caspase-3 expression levels. These results suggest that the neuroprotective mechanisms of liquiritin are connected to the regulation of metabolic disorders, activation Nrf2/Keap1 pathway, attenuation ERK1/2/NF-kappaB pathway, and inhibition mitochondrial apoptosis pathway.
- Journal
- Food Chem Toxicol
- Publish Year
- 2020
- Experiment Subject
- Experiment Type
- Cell Experiment
- Phenotype Related
- Metabolic Disorders
- Paper Title Cn
- Paper Title En
- Liquiritin protects PC12 cells from corticosterone-induced neurotoxicity via regulation of metabolic disorders, attenuation ERK1/2-NF-κB pathway, activation Nrf2-Keap1 pathway, and inhibition mitochondrial apoptosis pathway
- Bilingual Status
- semi_complete