The cell non-targeted metabolomics technique was used to investigate the potential mechanism of Caly-cosin-7--β-d-glucoside (CAG) against cell oxygen-glucose deprivation/reperfusion (OGD/R). The OGD/R-injured HT22 cell model was constructed. The cells were divided into control, OGD/R, Edaravone (EDA), CAG-L, CAG-M, and CAG-H groups. The protective effect of CAG on OGD/R-injured nerve cells and its potential mechanism was investigated by detecting ROS levels, apoptosis rate, glutamic acid (Glu), γ-aminobutyric acid (GABA), nitric oxide (NO), and combining with cell non-targeted metabolomics. The results showed that after OGD/R, ROS levels, apoptosis rate, Glu and NO concentrations were significantly increased, while the concentrations of GABA were decreased considerably, which improved in a dose-dependent manner after CAG intervention. Cell non-targeted metabolomics results showed that CAG can dramatically improve the metabolomic characteristics of OGD/R-injured HT22 cells. Through bioinformatics analysis and molecular docking, it was found that purine metabolism may be an important pathway for CAG to treat OGD/R injury, and key proteins screened may be important targets for improving OGD/R injury. Therefore, CAG may protect OGD/R-injured HT22 cells by inhibiting apoptosis and oxidative stress, improving energy supply and the metabolomic characteristics of OGD/R-injured HT22 cells by regulating purine metabolism.
Download full-text PDF |
Source |
|---|---|
| http://www.ncbi.nlm.nih.gov/pmc/articles/PMC11819903 | PMC |
| http://dx.doi.org/10.3390/molecules30030549 | DOI Listing |
Publication Analysis
Top Keywords
Similar Publications
The Cholinergic Receptor Nicotinic α3 Was Reduced in the Hippocampus of Early Cognitively Impaired Adult Male Mice and Upregulated by Nicotine and Cytisine in HT22 Cells.
Cells
February 2025
Advanced Research Center for Geriatric and Gerontology, Akita University, Akita 010-8543, Japan.
Ageing is a major risk factor for cognitive and physical decline, but its mechanisms remain poorly understood. This study aimed to detect early cognitive and physical changes, and to analyze the pathway involved by monitoring two groups of mice: a young and an adult group. The study has identified the types of molecules involved in the hippocampus.
View Article and Find Full Text PDFQ-Der: a next-generation CoQ10 analogue supercharging neuroprotection by combating oxidative stress and enhancing mitochondrial function.
Front Mol Biosci
February 2025
Department of Biomolecular Sciences, University of Urbino Carlo Bo, Urbino, Italy.
Background: Mitochondrial dysfunction and oxidative stress are central mechanisms in the progression of neurodegenerative diseases. This study first evaluated the toxicity of Q-Der (Q10-diacetate), a derivative of Coenzyme Q10, in HT22 hippocampal neurons under normal and oxidative stress conditions.
Methods: HT22 cells were treated with Q-Der at 2.
Neuroprotective effects of hirudin against cerebral ischemia-reperfusion injury via inhibition of CCL2-mediated ferroptosis and inflammatory pathways.
Brain Res Bull
March 2025
Department of Cerebrovascular Disease, Hainan General Hospital, Hainan Affiliated Hospital of Hainan Medical University, Haikou570311, Hainan, PR China. Electronic address:
Cerebral ischemia-reperfusion injury (CIRI) is a leading cause of neurological impairment in stroke, primarily correlated to oxidative stress, inflammation, and ferroptosis. This study investigates the neuroprotective effects of hirudin on CIRI, focusing on its role in modulating neuronal survival, oxidative stress, and ferroptosis markers through inhibition of CCL2. A middle cerebral artery occlusion (MCAO) model in mice and an oxygen-glucose deprivation/reoxygenation (OGD/R) model in HT22 cells were used to simulate ischemic conditions.
View Article and Find Full Text PDFAzilsartan Confers Protection Against Kainic Acid-Induced Hippocampal Neuron Damage by Upregulating Sirt3/Sod2 Pathway.
Dev Neurobiol
April 2025
Department of Pharmacy, Maternal and Child Health Hospital of Hubei Province, Wuhan City, Hubei Province, China.
Epilepsy refers to a diverse group of neurological pathologies, coupled with a significant worldwide impact. Azilsartan, an angiotensin receptor blocker, is broadly applied as an antihypertensive medication. Considering that the neuroprotective potential of Azilsartan has been newly documented, our work was committed to characterizing the association of Azilsartan with epilepsy and its possible mechanism.
View Article and Find Full Text PDFMEK1 inhibition ameliorates mitochondrial-dependent apoptosis induced by deltamethrin in mouse hippocampal neuron HT22 cells.
Toxicol In Vitro
March 2025
Department of Toxicology, School of Public Health, Guangxi Key Laboratory of Environment and Health Research, Guangxi Medical University, Nanning 530021, China; Guangxi Colleges and Universities Key Laboratory of Prevention and Control of Highly Prevalent Diseases, Guangxi Medical University, Nanning 530021, China. Electronic address:
Deltamethrin (DM), a widely used pyrethroid insecticide, has been increasingly recognized as a risk factor for neurodegeneration. However, the underlying mechanism is still far from clear. In this study, we investigated whether MEK1 is involved in DM-induced neurotoxicity and mediated mitochondrial-dependent apoptosis.
View Article and Find Full Text PDFWant AI Summaries of new PubMed Abstracts delivered to your In-box?
Enter search terms and have AI summaries delivered each week - change queries or unsubscribe any time!