ArticleThe Journal of pharmacology and experimental therapeutics2010
Inhibition of IkappaB kinase-beta protects dopamine neurons against lipopolysaccharide-induced neurotoxicity.
Article in The Journal of pharmacology and experimental therapeutics, 2010. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 48 papers.
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Who cites it
48 citing papers in PubMed, 89 citations in OpenAlex.
- Narrative Review "Dual Frontiers in Neurodegeneration: Pharmacological Synergies and Divergences in Parkinson's Disease and Type 2 Diabetes Mellitus".Cellular and molecular neurobiology · 2026Review
- Dapagliflozin Preserves Peripheral Nerve Structure and Reduces Neuropathic Damage in Streptozotocin-Induced Diabetic Peripheral Neuropathy.International journal of molecular sciences · 2025Article
- Article
- IκB kinase β (IKKβ): Structure, transduction mechanism, biological function, and discovery of its inhibitors.International journal of biological sciences · 2023Review
- Turmeronols (A and B) fromBioscience of microbiota, food and health · 2023Article
- Microglia as Therapeutic Target for Radiation-Induced Brain Injury.International journal of molecular sciences · 2022Review
- Neuroprotective and therapeutic effects of calcitriol in rotenone-induced Parkinson's disease rat model.Frontiers in cellular neuroscience · 2022Article
- Advances in Immunosuppressive Agents Based on Signal Pathway.Frontiers in pharmacology · 2022Review
- Fine Tuning of an Oxidative Stress Model with Sodium Iodate Revealed Protective Effect of NF-κB Inhibition and Sex-Specific Difference in Susceptibility of the Retinal Pigment Epithelium.Antioxidants (Basel, Switzerland) · 2021Article
- Insulin Signaling as a Therapeutic Target in Glaucomatous Neurodegeneration.International journal of molecular sciences · 2021Review
- Physiological Concentration of HCellular and molecular neurobiology · 2021Article
- Lipopolysaccharide-Induced Neuroinflammation as a Bridge to Understand Neurodegeneration.International journal of molecular sciences · 2019Review
- Icariin attenuates neuroinflammation and exerts dopamine neuroprotection via an Nrf2-dependent manner.Journal of neuroinflammation · 2019Article
- Naringenin Produces Neuroprotection Against LPS-Induced Dopamine Neurotoxicity via the Inhibition of Microglial NLRP3 Inflammasome Activation.Frontiers in immunology · 2019Article
- Interleukin-1 Beta and Tumor Necrosis Factor Alpha Upregulation and Nuclear Factor Kappa B Activation in Skeletal Muscle from a Mouse Model of Chronic/Progressive Parkinson Disease.Medical science monitor : international medical journal of experimental and clinical research · 2018Article
- Targeting IKKβ in Cancer: Challenges and Opportunities for the Therapeutic Utilisation of IKKβ Inhibitors.Cells · 2018Review
- Dual modulation on glial cells by tetrahydroxystilbene glucoside protects against dopamine neuronal loss.Journal of neuroinflammation · 2018Article
- Neutrophil-Based Drug Delivery Systems.Advanced materials (Deerfield Beach, Fla.) · 2018Review
- Taurine protects noradrenergic locus coeruleus neurons in a mouse Parkinson's disease model by inhibiting microglial M1 polarization.Amino acids · 2018Article
- Targeting MAPK Pathways by Naringenin Modulates Microglia M1/M2 Polarization in Lipopolysaccharide-Stimulated Cultures.Frontiers in cellular neuroscience · 2018Article
Corrections and comments
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Authors and funding
6 authors at 2 institutions in 2 countries.
Funding
Abstract
Parkinson's disease (PD) is a progressive neurological disorder characterized by a selective loss of dopamine (DA) neurons in the substantia nigra (SN). Although current therapy can control symptoms of this disorder, there is no effective therapy available to halt its progression. Recently, neuroinflammation has been recognized as an important contributor to the pathogenesis of PD, and nuclear factor-kappaB (NF-kappaB) plays a key role in regulating neuroinflammation. Hence, the modulation of NF-kappaB pathway may have therapeutic potential for PD. Activation of NF-kappaB depends on the phosphorylation of its inhibitor, IkappaB, by the specific IkappaB kinase (IKK) subunit IKK-beta. Compound A (7-[2-(cyclopropylmethoxy)-6-hydroxyphenyl]-5-[(3S)-3-piperidinyl]-1, 4-dihydro-2H-pyrido[2,3-d][1,3]oxazin-2-one hydrochloride), a potent and selective inhibitor of IKK-beta, has recently been reported to provide cardioprotection through specific suppression of NF-kappaB signaling. The present study, for the first time, elucidates neuroprotective effects of compound A. Daily subcutaneous injection of compound A (1 mg/kg) for 7 days inhibited the activation of microglia induced by nigral stereotaxic injection of lipopolysaccharide (LPS) and significantly attenuated LPS-induced loss of DA neurons in the SN. In vitro mechanistic studies revealed that neuroprotective effects of compound A were mediated by 1) suppressing the activity of microglial NADPH oxidase and decreasing the production of reactive oxygen species, and 2) inhibiting NF-kappaB-mediated gene transcription of various proinflammatory mediators in microglia via IKK-beta suppression. These findings indicate that compound A afforded potent neuroprotection against LPS-induced neurodegeneration through selective inhibition of NF-kappaB activation and may be of potential benefit in the treatment of PD.
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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.