ReferenceID 4133
Selaginella tamariscina Inhibits Glutamate-Induced Autophagic Cell Death by Activating the PI3K/AKT/mTOR Signaling Pathways
Int J Mol Sci
Glutamate-induced neural toxicity in autophagic neuron death is partially mediated by increased oxidative stress. Therefore, reducing oxidative stress in the brain is critical for treating or preventing neurodegenerative
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Record Fields
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- Reference Id
- 4133
- Evidence Id
- 20723
- Core Evidence Id
- 20723
- Source Reference Id
- 1555
- Herb2 Reference Id
- HBREF002352
- Subject Paper Key
- HERB003061_36232743
- Pubmed Id
- 36232743
- Doi
- 10.3390/ijms231911445
- Paper Title
- Selaginella tamariscina Inhibits Glutamate-Induced Autophagic Cell Death by Activating the PI3K/AKT/mTOR Signaling Pathways
- Paper Abstract
- Glutamate-induced neural toxicity in autophagic neuron death is partially mediated by increased oxidative stress. Therefore, reducing oxidative stress in the brain is critical for treating or preventing neurodegenerative diseases. Selaginella tamariscina is a traditional medicinal plant for treating gastrointestinal bleeding, hematuria, leucorrhea, inflammation, chronic hepatitis, gout, and hyperuricemia. We investigate the inhibitory effects of Selaginella tamariscina ethanol extract (STE) on neurotoxicity and autophagic cell death in glutamate-exposed HT22 mouse hippocampal cells. STE significantly increased cell viability and mitochondrial membrane potential and decreased the expression of reactive oxygen species, lactate dehydrogenase release, and cell apoptosis in glutamate-exposed HT22 cells. In addition, while glutamate induced the excessive activation of mitophagy, STE attenuated glutamate-induced light chain (LC) 3 II and Beclin-1 expression and increased p62 expression. Furthermore, STE strongly enhanced the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (Akt)/mammalian target of rapamycin (mTOR) phosphorylation activation. STE strongly inhibited glutamate-induced autophagy by activating the PI3K/Akt/mTOR signaling pathway. In contrast, the addition of LY294002, a PI3K/Akt inhibitor, remarkably suppressed cell viability and p -Akt and p62 expression, while markedly increasing the expression of LC3 II and Beclin-1. Our findings indicate that autophagy inhibition by activating PI3K/Akt/mTOR phosphorylation levels could be responsible for the neuroprotective effects of STE on glutamate neuronal damage.
- Journal
- Int J Mol Sci
- Publish Year
- 2022
- Experiment Subject
- mouse; glutamate-exposed ht22 cells; glutamate-exposed ht22 mouse hippocampal cells
- Experiment Type
- Animal Experiment
- Phenotype Related
- Inflammation; Chronic Hepatitis; Leucorrhea; Neurodegenerative Diseases; Gastrointestinal Bleeding; Hematuria; Gout; Hyperuricemia
- Paper Title Cn
- Paper Title En
- Selaginella tamariscina Inhibits Glutamate-Induced Autophagic Cell Death by Activating the PI3K/AKT/mTOR Signaling Pathways
- Bilingual Status
- semi_complete