ReferenceID 5210
Neuroprotective Studies of Evodiamine in an Okadaic Acid-Induced Neurotoxicity
Int J Mol Sci
BACKGROUND: Alzheimer's disease (AD) is the most common neurodegenerative disease, and it manifests as progressive memory loss and cognitive decline. However, there are no effective therapies for AD, which is an urgent p
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- Reference Id
- 5210
- Evidence Id
- 21800
- Core Evidence Id
- 21800
- Source Reference Id
- 3700
- Herb2 Reference Id
- HBREF004497
- Subject Paper Key
- HBIN026264_34069531
- Pubmed Id
- 34069531
- Doi
- 10.3390/ijms22105347
- Paper Title
- Neuroprotective Studies of Evodiamine in an Okadaic Acid-Induced Neurotoxicity
- Paper Abstract
- BACKGROUND: Alzheimer's disease (AD) is the most common neurodegenerative disease, and it manifests as progressive memory loss and cognitive decline. However, there are no effective therapies for AD, which is an urgent problem to solve. Evodiamine, one of the main bioactive ingredients of Evodia rutaecarpa, has been reported to ameliorate blood-brain barrier (BBB) permeability and improve cognitive impairment in ischemia and AD mouse models. However, whether evodiamine alleviates tauopathy remains unclear. This study aimed to examine whether evodiamine ameliorates tau phosphorylation and cognitive deficits in AD models. METHODS: A protein phosphatase 2A inhibitor, okadaic acid (OA), was used to induce tau phosphorylation to mimic AD-like models in neuronal cells. Protein expression and cell apoptosis were detected using Western blotting and flow cytometry, respectively. Spatial memory/cognition was assessed using water maze, passive avoidance tests, and magnetic resonance imaging assay in OA-induced mice models, and brain slices were evaluated further by immunohistochemistry. RESULTS: The results showed that evodiamine significantly reduced the expression of phosphor-tau, and further decreased tau aggregation and neuronal cell death in response to OA treatment. This inhibition was found to be via the inhibition of glycogen synthase kinase 3beta, cyclin-dependent kinase 5, and mitogen-activated protein kinase pathways. In vivo results indicated that evodiamine treatment ameliorated learning and memory impairments in mice, whereas Western blotting and immunohistochemical analysis of the mouse brain also confirmed the neuroprotective effects of evodiamine. CONCLUSIONS: Evodiamine can decrease the neurotoxicity of tau aggregation and exhibit a neuroprotective effect. Our results demonstrate that evodiamine has a therapeutic potential for AD treatment.
- Journal
- Int J Mol Sci
- Publish Year
- 2021
- Experiment Subject
- mouse
- Experiment Type
- Animal Experiment
- Phenotype Related
- Progressive Memory Loss; Alzheimer's Disease; Cognitive Impairment; Neurodegenerative Disease; Ischemia; Cognitive Decline; Cognitive Deficits
- Paper Title Cn
- Paper Title En
- Neuroprotective Studies of Evodiamine in an Okadaic Acid-Induced Neurotoxicity
- Bilingual Status
- semi_complete