Melatonin and Selenium Suppress Docetaxel-Induced TRPV1 Activation, Neuropathic Pain and Oxidative Neurotoxicity in Mice

Ertilav, Kemal; Nazıroğlu, Mustafa; Ataızı, Zeki Serdar; Yıldızhan, Kenan

doi:10.1007/s12011-020-02250-4

Cited by 25 publications

(12 citation statements)

References 64 publications

Supporting

Mentioning

Contrasting

Unclassified

Order By: Relevance

“…However, in animal experiments, the expression levels of Atp6v0a1 were upregulated by NGF, indicating that the expression of Atp6v0a1 was dependent on NGF ( Figure 3 ). We speculate that the differences between in vivo experiments and in vitro experiments may be due to: (1) Although SH-SY5Y cells have been used as an in vitro model in previous studies investigating pain mechanisms [ 25 , 26 , 27 ], differences between SH-SY5Y cells and trigeminal ganglion neurons exist. (2) The response of cells in vitro is different from that in the in vivo system, and the in vitro environment cannot fully simulate the effect of NGF on TG neurons during orofacial pain induced by experimental tooth movement in rats.…”

Section: Discussionmentioning

confidence: 99%

NGF-Induced Upregulation of CGRP in Orofacial Pain Induced by Tooth Movement Is Dependent on Atp6v0a1 and Vesicle Release

Tao

Liu

Lai

et al. 2022

IJMS

View full text Add to dashboard Cite

The nerve growth factor (NGF) and calcitonin gene-related peptide (CGRP) play a crucial role in the regulation of orofacial pain. It has been demonstrated that CGRP increases orofacial pain induced by NGF. V-type proton ATPase subunit an isoform 1 (Atp6v0a1) is involved in the exocytosis pathway, especially in vesicular transport in neurons. The objective was to examine the role of Atp6v0a1 in NGF-induced upregulation of CGRP in orofacial pain induced by experimental tooth movement. Orofacial pain was elicited by ligating closed-coil springs between incisors and molars in Sprague–Dawley rats. Gene and protein expression levels were determined through real-time polymerase chain reaction, immunostaining, and fluorescence in situ hybridization. Lentivirus vectors carrying Atp6v0a1 shRNA were used to knockdown the expression of Atp6v0a1 in TG and SH-SY5Y neurons. The release of vesicles in SH-SY5Y neurons was observed by using fluorescence dye FM1-43, and the release of CGRP was detected by Enzyme-Linked Immunosorbent Assy. Orofacial pain was evaluated through the rat grimace scale. Our results revealed that intraganglionic administration of NGF and Atp6v0a1 shRNA upregulated and downregulated CGRP in trigeminal ganglia (TG) and trigeminal subnucleus caudalis (Vc), respectively, and the orofacial pain was also exacerbated and alleviated, respectively, following administration of NGF and Atp6v0a1 shRNA. Besides, intraganglionic administration of NGF simultaneously caused the downregulation of Atp6v0a1 in TG. Moreover, the release of vesicles and CGRP in SH-SY5Y neurons was interfered by NGF and Atp6v0a1 shRNA. In conclusion, in the orofacial pain induced by experimental tooth movement, NGF induced the upregulation of CGRP in TG and Vc, and this process is dependent on Atp6v0a1 and vesicle release, suggesting that they are involved in the transmission of nociceptive information in orofacial pain.

show abstract

Section: Discussionmentioning

confidence: 99%

NGF-Induced Upregulation of CGRP in Orofacial Pain Induced by Tooth Movement Is Dependent on Atp6v0a1 and Vesicle Release

Tao

Liu

Lai

et al. 2022

IJMS

View full text Add to dashboard Cite

show abstract

“…In primary cultures of mouse DRG neurons, the inhibition of TRPV1 with specific blockers, such as capsaicin or resiniferatoxin, reduces the prooxidant capacity of microglial neurotoxicity (Ma et al, 2009 ). In addition, TRPV1 mediates vanilloid- and low pH-induced neurotoxicity in cultured rat cortical neurons (Shirakawa et al, 2007 ; Ertilav et al, 2021 ). In contrast, the inhibition of TRPV1 by the antagonist capsazepine attenuates its neuroprotective effects, indicating that TRPV1 activation contributes to the survival of rat nigral neurons (Park et al, 2012 ).…”

Section: The Effects Of Ca 2+ On Neurotoxicitymentioning

confidence: 99%

Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits

Guan

Cao

Yang

et al. 2021

Front. Mol. Neurosci.

View full text Add to dashboard Cite

Alzheimer’s disease (AD) is a neurodegenerative disease that is characterized by the production and deposition of β-amyloid protein (Aβ) and hyperphosphorylated tau, leading to the formation of β-amyloid plaques (APs) and neurofibrillary tangles (NFTs). Although calcium ions (Ca2+) promote the formation of APs and NFTs, no systematic review of the mechanisms by which Ca2+ affects the development and progression of AD has been published. Therefore, the current review aimed to fill the gaps between elevated Ca2+ levels and the pathogenesis of AD. Specifically, we mainly focus on the molecular mechanisms by which Ca2+ affects the neuronal networks of neuroinflammation, neuronal injury, neurogenesis, neurotoxicity, neuroprotection, and autophagy. Furthermore, the roles of Ca2+ transporters located in the cell membrane, endoplasmic reticulum (ER), mitochondria and lysosome in mediating the effects of Ca2+ on activating neuronal networks that ultimately contribute to the development and progression of AD are discussed. Finally, the drug candidates derived from herbs used as food or seasoning in Chinese daily life are summarized to provide a theoretical basis for improving the clinical treatment of AD.

show abstract

“…Furthermore, MLT reduces TRPV1 channel-induced neuronal death due to its neuroprotective activity in the DRGs of diabetic rats . Taxol-induced increases in TRPV1 channel expression levels, neuropathic pain, and neurotoxicity were reduced by MLT treatments . A combination of chemotherapeutic agent and MLT offers a potential therapy for breast cancer by increasing TRPV1 activity .…”

Section: Introductionmentioning

confidence: 96%

“…19 Taxol-induced increases in TRPV1 channel expression levels, neuropathic pain, and neurotoxicity were reduced by MLT treatments. 20 A combination of chemotherapeutic agent and MLT offers a potential therapy for breast cancer by increasing TRPV1 activity. 21 Therefore, it is of interest to determine whether MLT/MT2 results in the inhibition of the pRSK2/ pNEK2/JMJD3/TRPV1 pathway and attenuation of PTXinduced neuropathic pain.…”

Section: ■ Introductionmentioning

confidence: 99%

Melatonin Relieves Paclitaxel-Induced Neuropathic Pain by Regulating pNEK2-Dependent Epigenetic Pathways in DRG Neurons

Hsieh,

Lai,

Lin

et al. 2023

ACS Chem. Neurosci.

View full text Add to dashboard Cite

The neurohormone melatonin (MLT) demonstrates promising potential in ameliorating neuropathic pain induced by paclitaxel (PTX) chemotherapy. However, little is known about its protective effect on dorsal root ganglion (DRG) neurons in neuropathic pain resulting from the chemotherapeutic drug PTX. Here, PTX-treated rats revealed that intrathecal administration of MLT dose-dependently elevated hind paw withdrawal thresholds and latency, indicating that MLT significantly reversed PTX-induced neuropathic pain. Mechanistically, the analgesic effects of MLT were found to be mediated via melatonin receptor 2 (MT2), as pretreatment with an MT2 receptor antagonist inhibited these effects. Moreover, intrathecal MLT injection reversed the pNEK2-dependent epigenetic program induced by PTX. All of the effects caused by MLT were blocked by pretreatment with an MT2 receptor-selective antagonist, 4P-PDOT. Remarkably, multiple MLT administered during PTX treatment (PTX+MLTs) exhibited not only rapid but also lasting reversal of allodynia/hyperalgesia compared to single-bolus MLT administered after PTX treatment (PTX+MLT). In addition, PTX+MLTs exhibited greater efficacy in reversing PTX-induced alterations in pRSK2, pNEK2, JMJD3, H3K27me3, and TRPV1 expression and interaction in DRG neurons than PTX+MLT. These results indicated that MLT administered during PTX treatment reduced the incidence and/or severity of neuropathy and had a better inhibitory effect on the pNEK2-dependent epigenetic program compared to MLT administered after PTX treatment. In conclusion, MLT/MT2 is a promising therapy for the treatment of pNEK2-dependent painful neuropathy resulting from PTX treatment. MLT administered during PTX chemotherapy may be more effective in the prevention or reduction of PTX-induced neuropathy and maintaining quality.

show abstract

Melatonin and Selenium Suppress Docetaxel-Induced TRPV1 Activation, Neuropathic Pain and Oxidative Neurotoxicity in Mice

Cited by 25 publications

References 64 publications

NGF-Induced Upregulation of CGRP in Orofacial Pain Induced by Tooth Movement Is Dependent on Atp6v0a1 and Vesicle Release

NGF-Induced Upregulation of CGRP in Orofacial Pain Induced by Tooth Movement Is Dependent on Atp6v0a1 and Vesicle Release

Calcium Ions Aggravate Alzheimer’s Disease Through the Aberrant Activation of Neuronal Networks, Leading to Synaptic and Cognitive Deficits

Melatonin Relieves Paclitaxel-Induced Neuropathic Pain by Regulating pNEK2-Dependent Epigenetic Pathways in DRG Neurons

Contact Info

Product

Resources

About