ArticleThe Kaohsiung journal of medical sciences2023
Kaempferol counteracts bupivacaine-induced neurotoxicity in mouse dorsal root ganglia neurons by regulating TRAF6-dependent NF-κB signaling.
Article in The Kaohsiung journal of medical sciences, 2023. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 6 papers, 1 of them a synthesis that pooled it.
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Who cites it
6 citing papers in PubMed, 1 synthesis or guideline pooled it, 5 citations in OpenAlex.
- Bibliometric and visual analysis of global publications on kaempferol.Frontiers in nutrition · 2024Pooled it
- Phytocompounds Targeting Signaling Pathways in Stroke: Preclinical and Clinical Insights into Therapeutic Mechanisms and Neurotoxicity.Molecular neurobiology · 2026Review
- Targeting neuroimmune interactions: the therapeutic potential of kaempferol in immune-related central nervous system disorders.Frontiers in immunology · 2026Review
- The Impact of the Delivery Method on Oxidative Stress in Neonates: A Cross-Sectional Study.Journal of clinical medicine · 2025Article
- Inhibition of FOXO3 ameliorates ropivacaine-induced nerve cell damage through the miR-126-5p/TRAF6 axis.In vitro cellular & developmental biology. Animal · 2024Article
- 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
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Authors and funding
2 authors at 1 institution in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Kaempferol (KA), a widely recognized anti-oxidation and anti-inflammation agent, has been reported to have neuroprotective effects. This work aimed to investigate whether KA protects mouse dorsal root ganglia (DRG) neurons against bupivacaine (BU)-stimulated neurotoxicity and explore the underlying mechanisms. In this study, BU treatment suppressed DRG neuron viability and promoted LDH leakage, which was partially abated by KA. Besides, BU-triggered DRG neuron apoptosis, and changes in Bax and Bcl-2 levels were attenuated by KA treatment. In addition, pretreatment with KA substantially reduced interleukin (IL)-6, IL-1β, and tumor necrosis factor (TNF)-α levels in BU-treated DRG neurons. In addition, KA administration abrogated BU-induced decline in CAT, SOD, and GSH-Px levels, as well as the increase in the malondialdehyde level. Interestingly, we found that KA significantly attenuated BU-induced TNF receptor-associated factor 6 (TRAF6) upregulation as well as NF-κB activation. Furthermore, oe-TRAF6-mediated TRAF6 overexpression promoted NF-κB activation and partly abolished KA-induced protection against BU-triggered neurotoxic effects on DRG neurons. Our results revealed that KA mitigated BU-induced neurotoxic effects on DRG neurons by deactivating the TRAF6/NF-κB signaling.
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