ArticleNeurotoxicity research2018
Pristimerin Inhibits LPS-Triggered Neurotoxicity in BV-2 Microglia Cells Through Modulating IRAK1/TRAF6/TAK1-Mediated NF-κB and AP-1 Signaling Pathways In Vitro.
Article in Neurotoxicity research, 2018. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 27 papers.
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Who cites it
27 citing papers in PubMed, 40 citations in OpenAlex.
- Post-translational modifications in Neuroimmune cells during neuroinflammation: integrated regulatory networks and therapeutic opportunities.Biology direct · 2026Review
- The CEBPB-AP-1 (JunB/Fos) Axis Drives Neuroinflammation and Microglial Dysfunction Via TNF Signaling in Ischemic Stroke.Inflammation · 2026Article
- Pristimerin Dampens Acetaminophen-Induced Hepatotoxicity; The Role of NF-κB/iNOS/COX-II/Cytokines, PI3K/AKT, and BAX/BCL-2/Caspase-3 Signaling Pathways.Pharmaceutics · 2025Article
- Harnessing stem cell therapeutics in LPS-induced animal models: mechanisms, efficacies, and future directions.Stem cell research & therapy · 2025Review
- TheInternational journal of molecular sciences · 2025Article
- Aged-Related Changes in Microglia and Neurodegenerative Diseases: Exploring the Connection.Biomedicines · 2024Review
- Kaempferol counteracts bupivacaine-induced neurotoxicity in mouse dorsal root ganglia neurons by regulating TRAF6-dependent NF-κB signaling.The Kaohsiung journal of medical sciences · 2023Article
- Natural products in attenuating renal inflammationFrontiers in immunology · 2023Review
- Memory Impairment, Pro-Inflammatory Host Response and Brain Histopathologic Severity in Rats Infected withPathogens (Basel, Switzerland) · 2022Article
- Sesamin protects against neurotoxicity via inhibition of microglial activation under high glucose circumstances through modulating p38 and JNK signaling pathways.Scientific reports · 2022Article
- The Establishment of a Noninvasive Bioluminescence-Specific Viral Encephalitis Model by Pseudorabies Virus-Infected NF-κBp-Luciferase Mice.Veterinary sciences · 2022Article
- AQP4 Attenuated TRAF6/NFκB Activation in Acrylamide-Induced Neurotoxicity.Molecules (Basel, Switzerland) · 2022Article
- Protective Effect of Rifampicin Loaded by HPMA-PLA Nanopolymer on Macrophages Infected with Mycobacterium Tuberculosis.Computational and mathematical methods in medicine · 2022Article
- Sodium P-aminosalicylic Acid Inhibits Manganese-Induced Neuroinflammation in BV2 Microglial Cells via NLRP3-CASP1 Inflammasome Pathway.Biological trace element research · 2021Article
- Pristimerin protects against inflammation and metabolic disorder in mice through inhibition of NLRP3 inflammasome activation.Acta pharmacologica Sinica · 2021Article
- miR‑146a reduces depressive behavior by inhibiting microglial activation.Molecular medicine reports · 2021Article
- NVP-BEZ235 Inhibits Renal Cell Carcinoma by Targeting TAK1 and PI3K/Akt/mTOR Pathways.Frontiers in pharmacology · 2021Article
- Argon reduces microglial activation and inflammatory cytokine expression in retinal ischemia/reperfusion injury.Neural regeneration research · 2021Article
- Involvement of NFƙB and MAPK signaling pathways in the preventive effects of Ganoderma lucidum on the inflammation of BV-2 microglial cells induced by LPS.Journal of neuroimmunology · 2020Article
- Pristimerin Suppresses RANKL-Induced Osteoclastogenesis and Ameliorates Ovariectomy-Induced Bone Loss.Frontiers in pharmacology · 2020Article
Corrections and comments
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
Abstract
Microglia plays a prominent role in the brain's inflammatory response to injury or infection by migrating to affected locations and secreting inflammatory molecules. However, hyperactivated microglial is neurotoxic and plays critical roles in the pathogenesis of neurodegenerative diseases. Pristimerin, a naturally occurring triterpenoid, possesses antitumor, antioxidant, and anti-inflammatory activities. However, the effect and the molecular mechanism of pristimerin against lipopolysaccharide (LPS)-induced neurotoxicity in microglia remain to be revealed. In the present study, using BV-2 microglial cultures, we investigated whether pristimerin modifies neurotoxicity after LPS stimulation and which intracellular pathways are involved in the effect of pristimerin. Here we show that pristimerin markedly suppressed the release of Regulated on Activation, Normal T Expressed and Secreted (RANTES), transforming growth factor-β1 (TGF-β1), IL-6, tumor necrosis factor-α (TNF-α), and nitric oxide (NO). Pristimerin also significantly inhibited migration of BV-2 microglia and alleviated the death of neuron-like PC12 cell induced by the conditioned medium from LPS-activated BV-2 microglial cells. Moreover, pristimerin reduced the expression and interaction of TNF Receptor-Associated Factor 6 (TRAF6) and Interleukin-1 Receptor-Associated Kinases (IRAK1), limiting TGF-beta activating kinase 1 (TAK1) activation, and resulting in an inhibition of IKKα/β/NF-κB and MKK7/JNK/AP-1 signaling pathway in LPS-activated BV-2 microglia. Taken together, the anti-neurotoxicity action of pristimerin is mediated through the inhibition of TRAF6/IRAK1/TAK1 interaction as well as the related pathways: IKKα/β/NF-κB and MKK7/JNK/AP-1 signaling pathways. These findings may suggest that pristimerin might serve as a new therapeutic agent for treating hyperactivated microglial induced neurodegenerative diseases.
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