ArticleInternational journal of molecular sciences2020
Apamin Suppresses LPS-Induced Neuroinflammatory Responses by Regulating SK Channels and TLR4-Mediated Signaling Pathways.
Article in International journal of molecular sciences, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
What it found
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Who cites it
18 citing papers in PubMed, 30 citations in OpenAlex.
- Bee venom enhances dopaminergic function and behavioral recovery in a murine model of Parkinson's disease.Neuroprotection (Chichester, England) · 2026Article
- JAK/STAT signaling pathway inhibitors in neurodegenerative diseases: current status and future perspectives.Frontiers in aging neuroscience · 2026Review
- Fluoxetine alleviates postoperative cognitive dysfunction by attenuating TLR4/MyD88/NF-κB signaling pathway activation in aged mice.Inflammation research : official journal of the European Histamine Research Society ... [et al.] · 2023Article
- Protective Effects of Apamin on Acetaminophen-Induced Hepatotoxicity in Mice.Current issues in molecular biology · 2023Article
- Microglia activation in central nervous system disorders: A review of recent mechanistic investigations and development efforts.Frontiers in neurology · 2023Review
- Effects of Apamin on MPPInternational journal of molecular sciences · 2022Article
- Novel Nanoconjugate of Apamin and Ceftriaxone for Management of Diabetic Wounds.Life (Basel, Switzerland) · 2022Article
- Pharmacological effects and mechanisms of bee venom and its main components: Recent progress and perspective.Frontiers in pharmacology · 2022Review
- SK Channels Modulation Accelerates Equilibrium Recovery in Unilateral Vestibular Neurectomized Rats.Pharmaceuticals (Basel, Switzerland) · 2021Article
- Bee venom acupuncture therapy ameliorates neuroinflammatory alterations in a pilocarpine-induced epilepticus model.Metabolic brain disease · 2021Article
- Apamin Enhances Neurite Outgrowth and Regeneration after Laceration Injury in Cortical Neurons.Toxins · 2021Article
- Bee Venom-Derived BBB Shuttle and its Correlation with Oligodendrocyte Proliferation Markers in Mice Model of Multiple Sclerosis.Neurotoxicity research · 2021Article
- Anti-Neuroinflammatory Effects and Mechanism of Action ofPlants (Basel, Switzerland) · 2021Article
- Anti-Inflammatory Effect of Wasp Venom in BV-2 Microglial Cells in Comparison with Bee Venom.Insects · 2021Article
- Sorafenib Modulates the LPS- and Aβ-Induced Neuroinflammatory Response in Cells, Wild-Type Mice, and 5xFAD Mice.Frontiers in immunology · 2021Article
- Lipopolysaccharide Preparation Derived FromFrontiers in cellular and infection microbiology · 2021Article
- Antioxidative, Antiapoptotic, and Anti-Inflammatory Effects of Apamin in a Murine Model of Lipopolysaccharide-Induced Acute Kidney Injury.Molecules (Basel, Switzerland) · 2020Article
- Apamin administration impact on miR-219 and miR-155-3p expression in cuprizone induced multiple sclerosis model.Molecular biology reports · 2020Article
Corrections and comments
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Authors and funding
3 authors at 2 institutions in 1 country.
Funding
Abstract
Neuroinflammation plays a vital role in neurodegenerative conditions. Microglia are a key component of the neuroinflammatory response. There is a growing interest in developing drugs to target microglia and thereby control neuroinflammatory processes. Apamin (APM) is a specifically selective antagonist of small conductance calcium-activated potassium (SK) channels. However, its effect on neuroinflammation is largely unknown. We examine the effects of APM on lipopolysaccharide (LPS)-stimulated BV2 and rat primary microglial cells. Regarding the molecular mechanism by which APM significantly inhibits proinflammatory cytokine production and microglial cell activation, we found that APM does so by reducing the expression of phosphorylated CaMKII and toll-like receptor (TLR4). In particular, APM potently suppressed the translocation of nuclear factor kappa-light-chain-enhancer of activated B cells (NF-κB)/signal transducer and activator of transcription (STAT)3 and phosphorylated mitogen-activated protein kinases (MAPK)-extracellular signal-regulated kinase (ERK). In addition, the correlation of NF-κB/STAT3 and MAPK-ERK in the neuroinflammatory response was verified through inhibitors. The literature and our findings suggest that APM is a promising candidate for an anti-neuroinflammatory agent and can potentially be used for the prevention and treatment of various neurological disorders.
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Registered trials
Read under generation 80e0d062 · epoch 390. Bibliography from PubMed, PubMed Central and OpenAlex; grants from NIH RePORTER; trial links from ClinicalTrials.gov; estimates, votes and beliefs from the OpenQuestion graph.