Thiamine, riboflavin, and nicotinamide inhibit paclitaxel-induced allodynia by reducing TNF-α and CXCL-1 in dorsal root ganglia and thalamus and activating ATP-sensitive potassium channels

Braga, Alysson Vinícius; Costa, Sarah O.A.M.; Rodrigues, Felipe F.; Melo, Ivo S.F.; Morais, Marcela I.; Coelho, Márcio M.; Machado, Renes R.

doi:10.1007/s10787-019-00625-1

Cited by 25 publications

(21 citation statements)

References 69 publications

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“…Additionally, paclitaxel-induced peripheral neuropathy was attenuated by the selective Na v 1.7 and non-selective Na v 1.7-1.8 channel blockers ProTx II and ralfinamide, respectively (Li, North, et al, 2018; Liang, Yu, & Su, 2018). (Braga et al, 2019;Brito et al, 2018). These findings suggest that activators of Kv and K ATP channels might be effective alternatives to relief taxane-induced peripheral neuropathy.…”

Section: Sodium Channelsmentioning

confidence: 81%

“…For instance, H 2 S donors presented anti‐allodyinic activities in paclitaxel‐induced cold hypersensitivity in mice, a response that was attenuated by the Kv7 channel blocker XE991 (Di Cesare Mannelli et al, 2017). Additionally, the K ATP channel inhibitor glibenclamide reversed the antinociceptive actions of different compounds in paclitaxel‐induced peripheral neuropathy in mice (Braga et al, 2019; Brito et al, 2018). These findings suggest that activators of Kv and K ATP channels might be effective alternatives to relief taxane‐induced peripheral neuropathy.…”

Section: Taxane‐induced Peripheral Neuropathymentioning

confidence: 99%

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Taxane‐induced neurotoxicity: Pathophysiology and therapeutic perspectives

Costa

Passos

Quintão

et al. 2020

British J Pharmacology

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Taxane-derived drugs are antineoplastic agents used for the treatment of highly common malignancies. Paclitaxel and docetaxel are the most commonly used taxanes; however, other drugs and formulations have been used, such as cabazitaxel and nabpaclitaxel. Taxane treatment is associated with neurotoxicity, a well-known and relevant side effect, very prevalent amongst patients undergoing chemotherapy. Painful peripheral neuropathy is the most dose-limiting side effect of taxanes, affecting up to 97% of paclitaxel-treated patients. Central neurotoxicity is an emerging side effect of taxanes and it is characterized by cognitive impairment and encephalopathy. Besides impairing compliance to chemotherapy treatment, taxane-induced neurotoxicity (TIN) can adversely affect the patient's life quality on a long-term basis. Despite the clinical relevance, not many reviews have comprehensively addressed taxaneinduced neurotoxicity when they are used therapeutically. This article provides an up-to-date review on the pathophysiology of TIN and the novel potential therapies to prevent or treat this side effect. Abbreviations: Ca v , voltage-gated calcium; CB 1 , cannabinoid receptor 1; CB 2 , cannabinoid receptor 2; CCL2, chemokine (C-C motif) ligand 2; CCR2, CC motif chemokine receptor 2; CIPN, chemotherapy-induced peripheral neuropathy; CREB, cAMP response element-binding; CX3CL1, C-X3-C motif chemokine ligand 1; CXCL1, C-X3-C motif chemokine ligand 1; CXCL12, C-X-C motif chemokine ligand 12; CXCR1, C-X-C motif chemokine receptor 1; CXCR2, C-X-C motif chemokine receptor 2; DRG, dorsal root ganglion; GHS-R, growth hormone secretagogue receptor; IENFs, intra-epidermal nerve fibres; K ATP , ATP-sensitive potassium channel; K v , voltage-gated potassium channel; mPTP, mitochondrial permeability transition pore; Na v , voltage-gated sodium channel; Nrf2, nuclear factor-2 erythroid-related factor-2; PIPN, paclitaxel-induced peripheral neuropathy; TICN, taxane-induced central neurotoxicity; TIN, taxane-induced neurotoxicity; TIPN, taxane-induced peripheral neuropathy; TLR4, toll-like receptor-4; TRPA1, transient receptor potential cation channel subfamily A member 1; TRPV1, transient receptor potential cation channel subfamily V member 1; TRPV4, transient receptor potential cation channel subfamily V member 4.

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Section: Sodium Channelsmentioning

confidence: 81%

Section: Taxane‐induced Peripheral Neuropathymentioning

confidence: 99%

Taxane‐induced neurotoxicity: Pathophysiology and therapeutic perspectives

Costa

Passos

Quintão

et al. 2020

British J Pharmacology

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“…Mitochondrial dysfunction produces a bioenergetic deficit and nicotinamide riboside, a vitamin B3 precursor of NADþ, prevents paclitaxel-induced peripheral neuropathy by ameliorating the decreased levels of NAD þ in the sciatic nerve of paclitaxel-treated rats [31]. The B vitamins nicotinamide, thiamin, and riboflavin exhibit antinociceptive activity in paclitaxel-induced neuropathic pain and reduce inflammatory cytokines such as TNF-a in DRG [46]. Furthermore, paclitaxel reduces peroxisome proliferator-activated receptor gamma coactivator 1-alpha (PGC1a), a master regulator of mitochondrial biogenesis in sensory neurons [32,47] and expression of MFN2, a protein regulating mitochondrial transport and fusion [48].…”

Section: Mitochondrial Dysfunctionmentioning

confidence: 99%

Neuro-immune interactions in paclitaxel-induced peripheral neuropathy

et al. 2021

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Background: Paclitaxel is a taxane-based chemotherapeutic agent used as a treatment in breast cancer. There is no effective prevention or treatment strategy for the most common side effect of peripheral neuropathy. In this manuscript, we reviewed the molecular mechanisms that contribute to paclitaxel-induced peripheral neuropathy (PIPN) with an emphasis on immune-related processes. Methods: A systematic search of the literature was conducted in PubMed, EMBASE and Cochrane Library. The SYRCLE's risk of bias tool was used to assess internal validity. Results: 156 studies conducted with rodent models were included. The risk of bias was high due to unclear methodology. Paclitaxel induces changes in myelinated axons, mitochondrial dysfunction, and mechanical hypersensitivity by affecting ion channels expression and function and facilitating spinal transmission. Paclitaxel-induced inflammatory responses are important contributors to PIPN. Conclusion: Immune-related processes are an important mechanism contributing to PIPN. Studies in humans that validate these mechanistic data are highly needed to facilitate the development of therapeutic strategies.

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“…Vitamin B 1 or thiamine is essential for neuronal function especially in energy production, anti-nociception and cognitive performance ( Eisinger, 1997 ). Its deficiency in animals showed less brain glutamate, 2-oxo-glutarate and GABA ( Page et al, 1989 , Braga et al, 2020 ). Vitamin B 2 or riboflavin is essential for cellular metabolism, energy production, anti-nociception, as well as regulation of vitamins B 1 and B 3 .…”

Section: Application Of Nutrition In Depression Managementmentioning

confidence: 99%

“…Vitamin B 2 or riboflavin is essential for cellular metabolism, energy production, anti-nociception, as well as regulation of vitamins B 1 and B 3 . Its deficiency may affect the glycolysis pathway, as well as iron deficiency ( Braga et al, 2020 ). Vitamin B 3 or niacin is relevant in the production of serotonin, deficiency of vitamin B 3 results in negative effect on mood ( Bourre, 2006 ).…”

Section: Application Of Nutrition In Depression Managementmentioning

confidence: 99%

Nutritional therapy can reduce the burden of depression management in low income countries: A review

Ekong

Iniodu

2021

IBRO Neuroscience Reports

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Depression is a serious mental and mood disorder with global health and economic burden. This burden may be overwhelming in low income countries, although there are insufficient data. Most antidepressant formulations are predicated on the monoamine, neuroendocrine and neuro-inflammation hypotheses, with little or no cognizance to other neurochemicals altered in depression. A nutritional strategy with or without conventional antidepressants is recommended, as nutrition plays vital roles in the onset, severity and duration of depression, with poor nutrition contributing to its pathogenesis. This review discusses nutritional potentials of utilizing omega-3 fatty acids, proteins, vitamins, minerals and herbs or their phytochemicals in the management of depression with the aim of reducing depression burden. Literature search of empirical data in books and journals in data bases including but not limited to PubMed, Scopus, Science Direct, Web of Science and Google Scholar that might contain discussions of sampling were sought, their full text obtained, and searched for relevant content to determine eligibility. Omega-3 fatty and amino acids had significant positive anti-depression outcomes, while vitamins and minerals although essential, enhanced omega-3 fatty and amino acids activities. Some herbs either as whole extracts or their phytochemicals/metabolites had significant positive anti-depression efficacy. Nutrition through the application of necessary food classes or herbs as well as their phytochemicals, may go a long way to effectively manage depression. This therefore will provide inexpensive, natural, and non-invasive therapeutic means with reduced adverse effects that can also be applied alongside clinical management. This nutritional strategy should be given more attention in research, assessment and treatment for those with depression and other mental illness in low income countries, especially in Africa.

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Thiamine, riboflavin, and nicotinamide inhibit paclitaxel-induced allodynia by reducing TNF-α and CXCL-1 in dorsal root ganglia and thalamus and activating ATP-sensitive potassium channels

Cited by 25 publications

References 69 publications

Taxane‐induced neurotoxicity: Pathophysiology and therapeutic perspectives

Taxane‐induced neurotoxicity: Pathophysiology and therapeutic perspectives

Neuro-immune interactions in paclitaxel-induced peripheral neuropathy

Nutritional therapy can reduce the burden of depression management in low income countries: A review

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