Use of capsaicin as a model in the study of migraine: a literature review

2021 ◽  
Vol 3 (1) ◽  
pp. 1-5
Author(s):  
Raisa Ferreira Costa ◽  
Emanuela Paz Rosas ◽  
Daniela Araújo de Oliveira ◽  
Marcelo Moraes Valença

Capsaicin is able to induce mast cell degranulation, an event probably related to the pathophysiologyof a migraine attack. The present review study aimed to address the mechanisms of action of capsaicin and other chemical inducers in mast cell degranulation and an interaction of nerves and events that happen in the dura mater with the activation of mast cells. A survey was carried out in the literature, from 1980 to 2019, in different databases, using the following terms: capsaicin, mast cell and dura mater. 36 articles were selected for this review. Studies indicate that the main mechanisms of action of capsaicin are chemical induction through the activation of TRPV1 channels,allowing calcium influx into neurons in the trigeminal ganglion of the dura mater, activating mast cell degranulation, releasing pro-inflammatory (e.g., histamine, oxide nitric) and vasoactive (e.g., CGRP and substance P) substances. Therefore, the use of capsaicin may be a tool to be used in an animal model to better understand the pathophysiology of migraine. 

2021 ◽  
Author(s):  
Raisa Ferreira Costa ◽  
Emanuela Paz Rosas ◽  
Daniella Araújo de Oliveira ◽  
Marcelo Moraes Valença

Introduction: Capsaicin is able to induce mast cell degranulation, an event probably related to the pathophysiology of a migraine attack. Objectives: The present review study aimed to address the mechanisms of action of capsaicin and other chemical inducers in mast cell degranulation and an interaction of nerves and events that happen in the dura mater with the activation of mast cells. Design: A survey was carried out in the literature, from 1980 to 2019, in different databases (SciELO, U.S. National Library of Medicine and the National Institutes Health (PubMed) and Web of Science) using the following terms: capsaicin, mast cell and dura mater. Methods: 36 articles were selected for this review. The inclusion criteria were experimental model studies in rats that described the mechanisms of action of chemical inducers, including capsaicin. Results: Studies indicate that the main mechanisms of action of capsaicin are chemical induction through the activation of TRPV1 channels, allowing calcium influx into neurons in the trigeminal ganglion of the dura mater, activating mast cell degranulation, releasing pro-inflammatory (e.g., histamine, oxide nitric) and vasoactive (e.g., CGRP and substance P) substances. Conclusion: Therefore, the use of capsaicin may be a tool to be used in na animal model to better understand the pathophysiology of migraine.


2018 ◽  
Vol 212 ◽  
pp. 166-174 ◽  
Author(s):  
Travis V. Gulledge ◽  
Nicholas M. Collette ◽  
Emily Mackey ◽  
Stephanie E. Johnstone ◽  
Yasamin Moazami ◽  
...  

Cephalalgia ◽  
2012 ◽  
Vol 32 (4) ◽  
pp. 337-345 ◽  
Author(s):  
Michael Baun ◽  
Martin Holst Friborg Pedersen ◽  
Jes Olesen ◽  
Inger Jansen-Olesen

Background: Pituitary adenylate cyclase activating peptide-38 (PACAP-38) has been shown to induce migraine in migraineurs, whereas the related peptide vasoactive intestinal peptide (VIP) does not. In the present study we examine the hypothesis that PACAP-38 and its truncated version PACAP-27 but not VIP cause degranulation of mast cells in peritoneum and in dura mater. Methods: The degranulatory effects of PACAP-38, PACAP-27 and VIP were investigated by measuring the amount of N-acetyl-β-hexosaminidase released from isolated peritoneal mast cells and from dura mater attached to the skull of the rat in vitro. In peritoneal mast cells N-truncated fragments of PACAP-38 (PACAP(6–38), PACAP(16–38) and PACAP(28–38)) were also studied. To investigate transduction pathways involved in mast cell degranulation induced by PACAP-38, PACAP-27 and VIP, the phospholipase C inhibitor U-73122 and the adenylate cyclase inhibitor SQ 22536 were used. Results: The peptides induced degranulation of isolated peritoneal mast cells of the rat with the following order of potency: PACAP-38 = PACAP(6–38) = PACAP(16–38) » PACAP-27 = VIP = PACAP(28–38). In the dura mater we found that 10−5 M PACAP-38 was significantly more potent in inducing mast cell degranulation than the same concentration of PACAP-27 or VIP. Inhibition of intracellular mechanisms demonstrated that PACAP-38-induced degranulation is mediated by the phospholipase C pathway. Selective blockade of the PAC1 receptor did not attenuate degranulation. Conclusion: These findings correlate with clinical studies and support the hypothesis that mast cell degranulation is involved in PACAP-induced migraine. PACAP-38 has a much stronger degranulatory effect on rat peritoneal and dural mast cells than VIP and PACAP-27. The difference in potency between PACAP-38- and PACAP-27/VIP-induced peritoneal mast cell degranulation is probably not related to the PAC1 receptor but is caused by a difference in efficacy on phospholipase C.


1995 ◽  
Vol 40 (8) ◽  
pp. 1651-1658 ◽  
Author(s):  
Robert L. Barclay ◽  
Partosh K. Dinda ◽  
Gerald P. Morris ◽  
William G. Paterson

2021 ◽  
Vol 2021 ◽  
pp. 1-11
Author(s):  
Yihua Piao ◽  
Jingzhi Jiang ◽  
Zhiguang Wang ◽  
Chongyang Wang ◽  
Shan Jin ◽  
...  

Glaucocalyxin A (GLA) has various pharmacological effects like antioxidation, immune regulation, and antiatherosclerosis. Here, in this study, the effect and mechanism of GLA on mast cell degranulation were studied. The results of the anti-DNP IgE-mediated passive cutaneous anaphylaxis (PCA) showed that GLA dramatically inhibited PCA in vivo, as evidenced by reduced Evans blue extravasation and decreased ear thickness. In addition, GLA significantly reduced the release of histamine and β-hexosaminidase, calcium influx, cytokine (IL-4, TNF-α, IL-1β, IL-13, and IL-8) production in the RBL-2H3 (rat basophilic leukemia cells), and RPMCs (peritoneal mast cells) in vitro. Moreover, we further investigated the regulatory mechanism of GLA on antigen-induced mast cells by Western blot, which showed that GLA inhibited FcεRI-mediated signal transduction and invalidated the phosphorylation of Syk, Fyn, Lyn, Gab2, and PLC-γ1. In addition, GLA inhibited the recombinant mouse high mobility group protein B1- (HMGB1-) induced mast cell degranulation through limiting nuclear translocation of NF-κBp65. Treatment of mast cells with siRNA-HMGB1 significantly inhibited HMGB1 levels, as well as MyD88 and TLR4, decreased intracellular calcium levels, and suppressed the release of β-hexosaminidase. Meanwhile, GLA increased NrF2 and HO-1 levels by activating p38MAPK phosphorylation. Consequently, these data suggest that GLA regulates the NrF2/HO-1 signaling pathway through p38MAPK phosphorylation and inhibits HMGB1/TLR4/NF-κB signaling pathway to reduce mast cell degranulation and allergic inflammation. Our findings could be used as a promising therapeutic drug against allergic inflammatory disease.


2017 ◽  
Vol 104 (1) ◽  
pp. 15-24 ◽  
Author(s):  
E Kilinc ◽  
Y Dagistan ◽  
B Kotan ◽  
A Cetinkaya

In this study, we aimed to investigate the effects of Nigella sativa seeds and certain species of fungi extracts on the number and degranulation states of dural mast cells in rats. Rats were fed ad libitum with normal tap water or tap water with extract of N. sativa seed, Ramaria condensata, Lactarius salmonicolor, Lactarius piperatus, and Tricholoma terreum for 3 days. Mast cells in dura mater were counted and evaluated in terms of granulation and degranulation states. Compound 48/80, a mast cell degranulating agent, and T. terreum significantly increased the percent of degranulated mast cells in dura mater, respectively (p < 0.01 and p < 0.05). Moreover, T. terreum causes a significant increase in the total number of mast cells (p < 0.05). N. sativa significantly inhibited mast cell degranulation induced by both the compound 48/80 and T. terreum (p < 0.05), and significantly decreased the mast cell numbers increased by T. terreum (p < 0.05). Our results suggested that T. terreum following ingestion can contribute to headaches like migraine via dural mast cell degranulation and N. sativa may be able to exert analgesic and anti-inflammatory effects by stabilizing dural mast cells. However, investigation is needed to determine the ingredients of N. sativa that may be responsible for these beneficial effects.


2021 ◽  
Vol 12 ◽  
Author(s):  
Vikas P. Sukhatme ◽  
Angela M. Reiersen ◽  
Sharat J. Vayttaden ◽  
Vidula V. Sukhatme

Fluvoxamine is a well-tolerated, widely available, inexpensive selective serotonin reuptake inhibitor that has been shown in a small, double-blind, placebo-controlled, randomized study to prevent clinical deterioration of patients with mild coronavirus disease 2019 (COVID-19). Fluvoxamine is also an agonist for the sigma-1 receptor, through which it controls inflammation. We review here a body of literature that shows important mechanisms of action of fluvoxamine and other SSRIs that could play a role in COVID-19 treatment. These effects include: reduction in platelet aggregation, decreased mast cell degranulation, interference with endolysosomal viral trafficking, regulation of inositol-requiring enzyme 1α-driven inflammation and increased melatonin levels, which collectively have a direct antiviral effect, regulate coagulopathy or mitigate cytokine storm, which are known hallmarks of severe COVID-19.


Author(s):  
Ruth V.W. Dimlich

Mast cells in the dura mater of the rat may play a role in cerebral pathologies including neurogenic inflammation (vasodilation; plasma extravasation) and headache pain . As has been suggested for other tissues, dural mast cells may exhibit a close spatial relationship to nerves. There has been no detailed ultrastructural description of mast cells in this tissue; therefore, the goals of this study were to provide this analysis and to determine the spatial relationship of mast cells to nerves and other components of the dura mater in the rat.Four adult anesthetized male Wistar rats (290-400 g) were fixed by perfusion through the heart with 2% glutaraldehyde and 2.8% paraformaldehyde in a potassium phosphate buffer (pH 7.4) for 30 min. The head of each rat was removed and stored in fixative for a minimum of 24 h at which time the dural coverings were removed and dissected into samples that included the middle meningeal vasculature. Samples were routinely processed and flat embedded in LX 112. Thick (1 um) sections from a minimum of 3 blocks per rat were stained with toluidine blue (0.5% aqueous).


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