ReferenceID 6431
Trilobatin Protects Against Aβ25-35-Induced Hippocampal HT22 Cells Apoptosis Through Mediating ROS/p38/Caspase 3-Dependent Pathway
Front Pharmacol
Emerging evidence reveals that an aberrant accumulation of beta-amyloid (Abeta) is the main reason of Alzheimer's disease (AD) pathogenesis. Thus, inhibition of Abeta-induced neurotoxicity may be promising therapeutic ta
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Record Fields
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- Reference Id
- 6431
- Evidence Id
- 23021
- Core Evidence Id
- 23021
- Source Reference Id
- 6141
- Herb2 Reference Id
- HBREF006938
- Subject Paper Key
- HBIN047106_32508629
- Pubmed Id
- 32508629
- Doi
- 10.3389/fphar.2020.00584
- Paper Title
- Trilobatin Protects Against Aβ25-35-Induced Hippocampal HT22 Cells Apoptosis Through Mediating ROS/p38/Caspase 3-Dependent Pathway
- Paper Abstract
- Emerging evidence reveals that an aberrant accumulation of beta-amyloid (Abeta) is the main reason of Alzheimer's disease (AD) pathogenesis. Thus, inhibition of Abeta-induced neurotoxicity may be promising therapeutic tactics to mitigate AD onset and advance. The development of agent candidates by cultured neurons against Abeta-induced cytotoxicity is widely accepted to be an efficient strategy to explore the drug for AD patients. Previously, we have revealed that trilobatin (TLB), a small molecule monomer, derives from Lithocarpus polystachyus Rehd, possessed antioxidative activities on hydrogen peroxide-induced oxidative injury in PC12 cells. The present study was designed to investigate the effects and the underlying mechanism of TLB on Abeta-induced injury in hippocampal HT22 cells. The results demonstrated that TLB attenuated Abeta25-35-induced HT22 cell death, as evidenced by MTT assay and LDH release. Furthermore, TLB dramatically mitigated cell death after Abeta25-35 insulted via decreasing the intracellular and mitochondrial ROS overproduction and restoring antioxidant enzyme activities, as well as suppressing apoptosis. Of note, Abeta25-35 triggered increase in ratio of Bax/Bcl-2, activation of caspase-3, phosphorylation of tau, JNK, p38 MAPK, and decrease in Sirt3 expression, whereas TLB reversed these changes. Intriguingly, TLB could directly bind to p38, as evidenced by molecular docking and p38 inhibitor. Taken together, the results reveal that TLB effectively protects against Abeta25-35-induced neuronal cell death via activating ROS/p38/caspase 3-dependent pathway. Our findings afford evidence for the potential development of TLB to hinder neuronal death during AD.
- Journal
- Front Pharmacol
- Publish Year
- 2020
- Experiment Subject
- patient; cultured neurons; hippocampal ht22 cells; ht22 cell; pc12 cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- Neuronal Death; Alzheimer's Disease
- Paper Title Cn
- Paper Title En
- Trilobatin Protects Against Aβ25-35-Induced Hippocampal HT22 Cells Apoptosis Through Mediating ROS/p38/Caspase 3-Dependent Pathway
- Bilingual Status
- semi_complete