ArticleNeurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics2020
Levo-corydalmine Attenuates Vincristine-Induced Neuropathic Pain in Mice by Upregulating the Nrf2/HO-1/CO Pathway to Inhibit Connexin 43 Expression.
Article in Neurotherapeutics : the journal of the American Society for Experimental NeuroTherapeutics, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 30 papers.
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Who cites it
30 citing papers in PubMed, 53 citations in OpenAlex.
- Heme oxygenase/carbon monoxide system and cardiac conduction system.Medical gas research · 2026Review
- The Analgesic Effects of Nrf2 Activators in Chemotherapy-Induced Neuropathic Pain: Evidence from Animal Studies and Consequences for Translation into Clinical Trials.International journal of molecular sciences · 2026Review
- Review
- Da-Bu-Yin-Wan and Qian-Zheng-San Alleviate Parkinson's Disease by Activating the Keap1/Nrf2/HO-1 Pathway to Positively Regulate Oxidative Stress.CNS neuroscience & therapeutics · 2025Article
- The Double-Edged Effect of Connexins and Pannexins of Glial Cells in Central and Peripheral Nervous System After Nerve Injury.Molecular neurobiology · 2025Review
- Levo-corydalmine derived from Rhizoma Corydalis suppresses Ox-LDL-induced endothelial cell activation and improves vasodilatation by regulating the DDIT3-eNOS pathway.Naunyn-Schmiedeberg's archives of pharmacology · 2025Article
- Nrf2 Regulates Basal Glutathione Production in Astrocytes.International journal of molecular sciences · 2025Article
- Unlocking New Therapeutic Options for Vincristine-Induced Neuropathic Pain: The Impact of Preclinical Research.Life (Basel, Switzerland) · 2024Review
- RTA-408 Regulates p-NF-κB/TSLP/STAT5 Signaling to Ameliorate Nociceptive Hypersensitivity in Chronic Constriction Injury Rats.Molecular neurobiology · 2024Article
- From Plant to Chemistry: Sources of Active Opioid Antinociceptive Principles for Medicinal Chemistry and Drug Design.Molecules (Basel, Switzerland) · 2023Review
- CaMKII and CaCell biology and toxicology · 2023Article
- The Battlefield of Chemotherapy in Pediatric Cancers.Cancers · 2023Review
- 5,7-Dimethoxycoumarin ameliorates vincristine induced neuropathic pain: potential role of 5HTFrontiers in pharmacology · 2023Article
- Resolvin D1/N-formyl peptide receptor 2 ameliorates paclitaxel-induced neuropathic pain through the activation of IL-10/Nrf2/HO-1 pathway in mice.Frontiers in immunology · 2023Article
- The Interaction between Carbon Monoxide and Hydrogen Sulfide during Chronic Joint Pain in Young Female Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Neurodegeneration in Multiple Sclerosis: The Role of Nrf2-Dependent Pathways.Antioxidants (Basel, Switzerland) · 2022Review
- The Effects of Nuclear Factor Erythroid 2 (NFE2)-Related Factor 2 (Nrf2) Activation in Preclinical Models of Peripheral Neuropathic Pain.Antioxidants (Basel, Switzerland) · 2022Review
- The Beneficial Effects of Heme Oxygenase 1 and Hydrogen Sulfide Activation in the Management of Neuropathic Pain, Anxiety- and Depressive-like Effects of Paclitaxel in Mice.Antioxidants (Basel, Switzerland) · 2022Article
- Soluble epoxide hydrolase inhibition alleviates chemotherapy induced neuropathic pain.Frontiers in pain research (Lausanne, Switzerland) · 2022Article
- Chemotherapy-Induced Peripheral Neuropathy: Epidemiology, Pathomechanisms and Treatment.Oncology and therapy · 2021Review
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Authors and funding
10 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Antimicrotubulin chemotherapeutic agents, including plant-derived vincaalkaloids such as vincristine, can cause peripheral neuropathic pain. Exogenously activated heme oxygenase 1 (HO-1) is a potential therapy for chemotherapy-induced neuroinflammation. In this study, we investigated a role for Nrf2/HO-1/CO in mediating vincristine-induced neuroinflammation by inhibiting connexin 43 (Cx43) production in the spinal cord following the intrathecal application of the HO-1 inducer protoporphyrin IX cobalt chloride (CoPP) or inhibitor protoporphyrin IX zinc (ZnPP), and we analyzed the underlying mechanisms by which levo-corydalmine (l-CDL, a tetrahydroprotoberberine) attenuates vincristine-induced pain. Treatment with levo-corydalmine or oxycodone hydrochloride (a semisynthetic opioid analgesic, used as a positive control) attenuated vincristine-induced persistent pain hypersensitivity and degeneration of the sciatic nerve. In addition, the increased prevalence of atypical mitochondria induced by vincristine was ameliorated by l-CDL in both A-fibers and C-fibers. Next, we evaluated whether nuclear factor E2-related factor 2 (Nrf2), an upstream activator of HO-1, directly bound to the HO-1 promoter sequence and degraded heme to produce carbon monoxide (CO) following stimulation with vincristine. Notably, l-CDL dose-dependently increased HO-1/CO expression by activating Nrf2 to inhibit Cx43 expression in both the spinal cord and in cultured astrocytes stimulated with TNF-α, corresponding to decreased Cx43-mediated hemichannel. Furthermore, l-CDL had no effect on Cx43 following the silencing of the HO-1 gene. Taken together, our findings reveal a novel mechanism by which Nrf2/HO-1/CO mediates Cx43 expression in vincristine-induced neuropathic pain. In addition, the present findings suggest that l-CDL likely protects against nerve damage and attenuates vincristine-induced neuroinflammation by upregulating Nrf2/HO-1/CO to inhibit Cx43 expression.
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