ArticleDrug design, development and therapy2019
Monosialoganglioside protects against bupivacaine-induced neurotoxicity caused by endoplasmic reticulum stress in rats.
Article in Drug design, development and therapy, 2019. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 7 papers.
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Who cites it
7 citing papers in PubMed, 14 citations in OpenAlex.
- Molecular Mechanisms of Local Anesthetic Toxicity: From Ion Channel Dysregulation to Mitochondrial Dysfunction and Tissue-Specific Injury.International journal of molecular sciences · 2026Review
- Mitochondrial respiratory complex IV deficiency recapitulates amyotrophic lateral sclerosis.Nature neuroscience · 2025Article
- Drug-induced peripheral nerve palsy: a real-world study based on FAERS data from 2004 to the third quarter of 2024.Frontiers in pharmacology · 2025Article
- Resveratrol‑mediated activation of SIRT1 inhibits the PERK‑eIF2α‑ATF4 pathway and mitigates bupivacaine‑induced neurotoxicity in PC12 cells.Experimental and therapeutic medicine · 2023Article
- Review
- Resveratrol Suppresses Bupivacaine-Induced Spinal Neurotoxicity in Rats by Inhibiting Endoplasmic Reticulum Stress via SIRT1 Modulation.BioMed research international · 2023Article
- P53 and taurine upregulated gene 1 promotes the repair of the DeoxyriboNucleic Acid damage induced by bupivacaine in murine primary sensory neurons.Bioengineered · 2022Article
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Authors and funding
9 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
backgroundLocal anesthetics in spinal anesthesia have neurotoxic effects, resulting in severe neurological complications. Intrathecal monosialoganglioside (GM1) administration has a therapeutic effect on bupivacaine-induced neurotoxicity. The aim of this study was to determine the underlying mechanisms of bupivacaine-induced neurotoxicity and the potential neuroprotective role of GM1. MATERIALS AND
methodsA rat spinal cord neurotoxicity model was established by injecting bupivacaine (5%, 0.12 μL/g) intrathecally. The protective effect of GM1 (30 mg/kg) was evaluated by pretreating the animals with it prior to the bupivacaine regimen. The neurological and locomotor functions were assessed using standard tests. The histomorphological changes, neuron degeneration and apoptosis, and endoplasmic reticulum stress (ERS) relevant markers were analyzed using immunofluorescence, quantitative real-time PCR, and Western blotting.
resultsBupivacaine resulted in significant neurotoxicity in the form of aberrant neurolocomoter functions and spinal cord histomorphology and neuronal apoptosis. Furthermore, the ERS specific markers were significantly upregulated during bupivacaine-induced neurotoxicity. These neurotoxic effects were ameliorated by GM1.
conclusionPretreatment with GM1 protects against bupivacaine-induced neurotoxicity via the inhibition of the GRP78/PERK/eIF2α/ATF4-mediated ERS.
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