ReferenceID 5524
Isorhamnetin Attenuated the Release of Interleukin-6 from β-Amyloid-Activated Microglia and Mitigated Interleukin-6-Mediated Neurotoxicity
Oxid Med Cell Longev
Alzheimer's disease (AD), characterized by the abnormal accumulation of β -amyloid (A β ), is the most prevalent type of dementia, and it is associated with progressive cognitive decline and memory loss. A β accumulation
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Record Fields
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- Reference Id
- 5524
- Evidence Id
- 22114
- Core Evidence Id
- 22114
- Source Reference Id
- 4284
- Herb2 Reference Id
- HBREF005081
- Subject Paper Key
- HBIN031114_36160711
- Pubmed Id
- 36160711
- Doi
- 10.1155/2022/3652402
- Paper Title
- Isorhamnetin Attenuated the Release of Interleukin-6 from β-Amyloid-Activated Microglia and Mitigated Interleukin-6-Mediated Neurotoxicity
- Paper Abstract
- Alzheimer's disease (AD), characterized by the abnormal accumulation of β -amyloid (A β ), is the most prevalent type of dementia, and it is associated with progressive cognitive decline and memory loss. A β accumulation activates microglia, which secrete proinflammatory factors associated with A β clearance impairment and cause neurotoxicity, generating a vicious cycle among A β accumulation, activated microglia, and proinflammatory factors. Blocking this cycle can be a therapeutic strategy for AD. Using A β -activated HMC3 microglial cells, we observed that isorhamnetin, a main constituent of Oenanthe javanica , reduced the A β -triggered secretion of interleukin- (IL-) 6 and downregulated the expression levels of the microglial activation markers ionized calcium binding adaptor molecule 1 (IBA1) and CD11b and the inflammatory marker nuclear factor- κ B (NF- κ B). Treatment of the SH-SY5Y-derived neuronal cells with the A β -activated HMC3-conditioned medium (HMC3-conditioned medium) or IL-6 increased reactive oxygen species production, upregulated cleaved caspase 3 expression, and reduced neurite outgrowth, whereas treatment with isorhamnetin counteracted these neurodegenerative presentations. In the SH-SY5Y-derived neuronal cells, IL-6 upregulated the phosphorylation of tyrosine kinase 2 (TYK2) and signal transducer and activator of transcription 1 (STAT1), whereas isorhamnetin normalized this abnormal phosphorylation. Overexpression of TYK2 attenuated the neuroprotective effect of isorhamnetin on IL-6-induced neurotoxicity. Our findings demonstrate that isorhamnetin exerts its neuroprotective effect by mediating the neuroinflammatory IL-6/TYK2 signaling pathway, suggesting its potential for treating AD.
- Journal
- Oxid Med Cell Longev
- Publish Year
- 2022
- Experiment Subject
- a β -activated hmc3 microglial cells; sh-sy5y-derived neuronal cells
- Experiment Type
- Cell Experiment
- Phenotype Related
- A β clearance impairment; Dementia; Memory Loss; Cognitive Decline; Alzheimer's Disease
- Paper Title Cn
- Paper Title En
- Isorhamnetin Attenuated the Release of Interleukin-6 from β-Amyloid-Activated Microglia and Mitigated Interleukin-6-Mediated Neurotoxicity
- Bilingual Status
- semi_complete