Salmon calcitonin ameliorates migraine pain through modulation of <scp>CGRP</scp> release and dural mast cell degranulation in rats

Kılınç, Erkan; Dağıstan, Yaşar; Kükner, Aysel; Yılmaz, Bayram; Ağuş, Sami; Söyler, Gizem; Töre, Fatma

doi:10.1111/1440-1681.12915

Cited by 36 publications

(46 citation statements)

References 39 publications

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“…Finally, CGRP release in the meninges leads to vasodilation, mast cell degranulation, and neurogenic inflammation, mechanisms for migraine pain . Triptans prevent release of CGRP, interrupting this cascade …”

Section: Pathophysiologymentioning

confidence: 99%

“…11 Finally, CGRP release in the meninges leads to vasodilation, mast cell degranulation, and neurogenic inflammation, mechanisms for migraine pain. [12][13][14][15] Triptans prevent release of CGRP, interrupting this cascade. 16,17 These and other basic science studies led to CGRP assuming the role of target for migraine translational research.…”

Section: Pathophysiologymentioning

confidence: 99%

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History and Review of anti‐Calcitonin Gene‐Related Peptide (CGRP) Therapies: From Translational Research to Treatment

2018

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Objective – To briefly describe the history of and available data on anti‐calcitonin gene‐related peptide (CGRP) therapies for headache. Background – CGRP was proposed as a target for primary headache therapies. Translational research involved moving from delineating the relationships between CGRP and primary headaches and the clinical development of anti‐CGRP treatments. The first anti‐CGRP treatment, an intravenous CGRP‐receptor antagonist or gepant, olcegepant, was described as effective in terminating migraines in humans in 2004. Methods – The author briefly reviews some of the pathophysiology and translational research that led to the development of the gepants initially and then subsequently to the anti‐CGRP and anti‐CGRP receptor monoclonal antibodies. All accessible randomized controlled trials, abstracts, platform presentations, and press releases on the monoclonal antibody trials are summarized. The trajectory from bench research to the approval of the first anti‐CGRP receptor monoclonal antibody for clinical use in migraine prevention, erenumab, is discussed, as well as potential clinical uses of the anti‐CGRP treatments. Results – The US Food and Drug Administration (FDA) approved erenumab, an anti‐CGRP receptor monoclonal antibody, for prevention of migraine May 17, 2018. At the time of this writing (May 2018), 2 other anti‐CGRP monoclonal antibodies have been submitted to the FDA for the indication of prevention of migraine, galcanezumab and fremanezumab. Galcanezumab has reportedly shown effectiveness in preventing episodic cluster headache as well, although has not yet been submitted to the FDA for this indication. Eptinezumab will likely be submitted to the FDA for prevention of migraine later in 2018. Two gepants, ubrogepant and rimegepant, have completed positive pivotal trials for acute treatment of migraine, but have not yet been submitted to the FDA for this indication. Conclusions – The development of anti‐CGRP therapies opens a new era in the acute and preventive treatment of primary headache disorders.

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Section: Pathophysiologymentioning

confidence: 99%

Section: Pathophysiologymentioning

confidence: 99%

History and Review of anti‐Calcitonin Gene‐Related Peptide (CGRP) Therapies: From Translational Research to Treatment

2018

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“…Nitroglycerin is a nitric oxide donor and regarded to exhibit its migraine-like effects via activation of nitric oxide synthase enzyme. We recently demonstrated that nitroglycerin treatment enhanced degranulation of mast cells in the meninges in a nitroglycerininduced rat model of migraine (7). Inducer effect of nitroglycerin on degranulation of mast cells in the meninges was also shown by another group previously (16).…”

Section: Resultsmentioning

confidence: 69%

“…Degranulation of the mast cells in the meninges contribute to migraine pain by leading to neurogenic inflammation, and activation and sensitization of the trigeminovascular system (8). Experimental studies have shown that increased number and enhanced degranulation of mast cells in the meninges contribute to the generation and maintenance of migraine pain (1,5,7). It has been demonstrated that mast cell mediators including serotonin, prostaglandin-I2, and histamine lead to the sensitization and activation of the meningeal nociceptors (9).…”

Section: öZmentioning

confidence: 99%

Akciğer Mast Hücre Davranışının Migren Sıçan Modelinde İncelenişi: Migren Baş Ağrısı İçin Çıkarımlar

Kılınç

Balcı

2018

Anadolu Kliniği Tıp Bilimleri Dergisi

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In this study, we aimed to investigate the potential role of lung mast cells in migraine by using a nitroglycerin-induced migraine model in rats. Materials and Methods: Thirty-five adult male Wistar rats were divided into five groups. Each treatment being performed intraperitoneally, the NS group received 0.2 ml normal saline, the NTG group 10 mg/kg nitroglycerin, the NTG vehicle group 0.2 ml 0.1% ethanol in normal saline, the L-NAME+NTG group 50 mg/kg L-NAME + nitroglycerin, and the NS+NTG group normal saline + nitroglycerin. Two hours after the nitroglycerin and other treatments, the rats under anesthesia were intracardially perfused with a solution of 150 ml 4% paraformaldehyde. The lungs were harvested and stained with toluidine blue to observe mast cells. The data were analyzed by using one-way ANOVA. Results: Nitroglycerin increased significantly both number (from 94±3.8 to 131±6.7, p=0.0035) and percent of degranulation (from 11.8±1.3% to 35.5±5.7%, p=0.003) of lung mast cells. However, L-NAME prevented the effects of nitroglycerin on the number and degranulation of lung mast cells, attenuating the increase in both number (from 136±5.1 to 93±2.5, p=0.0011) and degranulation percentage of lung mast cells (from 37.3±1.0% to 13.6±3.1%, p=0.001) induced by nitroglycerin. Discussion and Conclusion: Our findings demonstrate that nitroglycerin treatment leads to an increase in the number and degranulation of lung mast cells in a rat model of migraine induced by nitroglycerin. Moreover, L-NAME prevented these effects, suggesting that nitric oxide released from nitroglycerin directly or indirectly leads to the activation of lung mast cells. The results obtained in the current study can pioneer new research on the role of lung mast cells in migraine.

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“…Normally activation of MCs is useful to establish homeostasis of body systems, but their over activation can chronically induce inflammatory responses such as in the case of asthma and arthritis (3). MCs participate in the inflammatory processes by releasing various pronociceptive, vasoactive and pro-inflammatory mediators from their granules through a process called degranulation (4). MCderived mediators such as serotonin, prostaglandin, histamine, tryptase, tumor necrosis factor-alpha (TNF-α), and interleukin (IL)-1β are able to trigger and enhance inflammatory reactions (5).…”

Section: Introductionmentioning

confidence: 99%

The comparison of effects of applications of compound 48/80 and mast cell mediator suspension on inflammation in rats: A methodological study for acute inflammatory pain

Kılınç¹,

Dağıstan²,

Çetinkaya³

et al. 2018

Clin Exp Health Sci

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Objective: Inflammation underlies the pathological basis of most diseases. Substance-P is a key mediator that participates in various inflammatory processes and painful conditions. Mast cells (MCs) have a key role in inflammatory processes via mediators released from their granules. The experimental models for the investigation of pathogenesis and treatment of inflammatory diseases represent merely certain characteristics of inflammatory cases, therefore, more comprehensive models are required. We aimed to compare effects of administrations of the compound-48/80 and mast cell mediator suspension (MCMS) obtained from peritoneal MCs on the inflammation in rats. Methods: Rats were divided into five groups (n=6): Intraperitoneally, Control group received 0.2 ml saline; C-48/80 group received 2 mg/kg compound-48/80; MCMS group received 0.2 ml MCMS; Cr+C-48/80 group received 10 mg/kg cromolyn plus compound-48/80; Cr+MCMS group received cromolyn plus MCMS. Potent inflammatory markers, plasma substance-P levels, and number and degranulation of dural MCs were measured. Data were analyzed using one-way ANOVA followed by Dunnett's post hoc test. Results: Compound-48/80 increased plasma substance-P levels (p<0.05) and dural MC-degranulation (p<0.001). Likewise, MCMS increased substance-P levels and dural MC-degranulation (p<0.001) as well as number of dural MCs (p<0.01). MC stabilizer cromolyn inhibited increases in the parameters induced by compound-48/80 and MCMS (p<0.01 and p<0.05, respectively). Conclusion: MCMS administration had greater impact to increase the plasma substance-P levels and number and degranulation of dural MCs than that of the compound-48/80 administration. The results demonstrate the potent inflammatory effect of MCMS treatment over the compund-48/80 administration. Administration of MCMS could be a useful tool to study inflammatory conditions.

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Salmon calcitonin ameliorates migraine pain through modulation of CGRP release and dural mast cell degranulation in rats

Cited by 36 publications

References 39 publications

History and Review of anti‐Calcitonin Gene‐Related Peptide (CGRP) Therapies: From Translational Research to Treatment

History and Review of anti‐Calcitonin Gene‐Related Peptide (CGRP) Therapies: From Translational Research to Treatment

Akciğer Mast Hücre Davranışının Migren Sıçan Modelinde İncelenişi: Migren Baş Ağrısı İçin Çıkarımlar

The comparison of effects of applications of compound 48/80 and mast cell mediator suspension on inflammation in rats: A methodological study for acute inflammatory pain

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