Inhibition of ovalbumin-induced allergic rhinitis by sumatriptan through the nitric oxide pathway in mice

Hemmati, Sara; Rahimi, Nastaran; Dabiri, Sasan; Alaeddini, Mojgan; Etemad‐Moghadam, Shahroo; Dehpour, Ahmad Reza

doi:10.1016/j.lfs.2019.116901

Cited by 16 publications

(13 citation statements)

References 45 publications

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“…Consistently, Buzzi et al revealed that sumatriptan can hider mast cell, endothelial, platelet activation after trigeminal activation (Buzzi et al, 1992). Our recent study on the rat model of ovalbumin‐induced rhinitis depicted the potential of sumatriptan to suppress the inflammation during rhinitis (Hemmati et al, 2019). Sumatriptan (3 μg/kg) decreased the scratching behavior and relieved the signs of inflammation including reduction of IL‐4 and serum IgE levels and elevation of interferon (IFN)‐γ levels (Hemmati et al, 2019).…”

Section: Resultsmentioning

confidence: 99%

“…Our recent study on the rat model of ovalbumin‐induced rhinitis depicted the potential of sumatriptan to suppress the inflammation during rhinitis (Hemmati et al, 2019). Sumatriptan (3 μg/kg) decreased the scratching behavior and relieved the signs of inflammation including reduction of IL‐4 and serum IgE levels and elevation of interferon (IFN)‐γ levels (Hemmati et al, 2019). Histological assessments also revealed that sumatriptan reduced eosinophil count in the nasal mucosa.…”

Section: Resultsmentioning

confidence: 99%

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Beyond its anti‐migraine properties, sumatriptan is an anti‐inflammatory agent: A systematic review

Ala

Ghasemi

Jafari

et al. 2021

Drug Development Research

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Sumatriptan is the first available medication from triptans family that was approved by the U.S. Food and Drug Administration for migraine attacks and cluster headaches in 1991. Most of its action is mediated by selective 5‐HT1B/1D receptor agonism. Recent investigations raised the possibility of repositioning of this drug to other indications beyond migraine, as increasing evidence suggests for an anti‐inflammatory property of sumatriptan. We performed a literature search using PubMed, Web of Science, Scopus, and Google Scholar using “inflammation AND sumatriptan” or “inflammation AND 5HT1B/D” as the keywords. Then, articles were screened for their relevance and those directly discussing the correlation between inflammation and sumatriptan or 5HT1B/D were included. Total references reviewed or inclusion/exclusion were 340 retrieved full‐text articles (n = 340), then based on critical assessment 66 of them were included in this systematic review. Our literature review indicates that at low doses, sumatriptan can reduce inflammatory markers (e.g., interleukin‐1β, tumor necrosis factor‐α, and nuclear factor‐κB), affects caspases and changes cells lifespan. Additionally, nitric oxide synthase and nitric oxide signaling seem to be regulated by this drug. It also inhibits the release of calcitonin gene‐related peptide. Sumatriptan protects against many inflammatory conditions including cardiac and mesenteric ischemia/reperfusion, skin flap, pruritus, peripheral, and central nervous system injuries such as spinal cord injury, testicular torsion‐detorsion, oral mucositis, and other experimental models. Considering the safety and potency of low dose sumatriptan compared to corticosteroids and other immunosuppressive medications, it is worth to take advantage of sumatriptan in inflammatory conditions.

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Section: Resultsmentioning

confidence: 99%

Section: Resultsmentioning

confidence: 99%

Beyond its anti‐migraine properties, sumatriptan is an anti‐inflammatory agent: A systematic review

Ala

Ghasemi

Jafari

et al. 2021

Drug Development Research

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“…Pilocarpine, lithium chloride, sumatriptan, GR‐127935, scopolamine methyl bromide, L‐NAME, 7‐nitroindazole, aminoguanidine, ketamine, and xylazine were injected intraperitoneally (i.p.). The doses of drugs, route of administration, and the time of injection were selected based on previous experiments, our pilot studies, and pharmacokinetic consideration [20,23,27,31].…”

Section: Methodsmentioning

confidence: 99%

Sumatriptan reduces severity of status epilepticus induced by lithium–pilocarpine through nitrergic transmission and 5‐HT_1B/D receptors in rats: A pharmacological‐based evidence

Eslami

Rahimi

Ostovaneh

et al. 2020

Fundamemntal Clinical Pharma

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Status epilepticus (SE) is a life‐threatening neurologic disorder that can be as both cause and consequence of neuroinflammation. In addition to previous reports on anti‐inflammatory property of the anti‐migraine medication sumatriptan, we have recently shown its anticonvulsive effects on pentylenetetrazole‐induced seizure in mice. In the present study, we investigated further (i) the effects of sumatriptan in the lithium–pilocarpine SE model in rats, and (ii) the possible involvement of nitric oxide (NO), 5‐hydroxytryptamin 1B/1D (5‐HT1B/1D) receptor, and inflammatory pathways in such effects of sumatriptan. Status epilepticus was induced by lithium chloride (127 mg/kg, i.p) and pilocarpine (60 mg/kg, i.p.) in Wistar rats. While SE induction increased SE scores and mortality rate, sumatriptan (0.001‐1 mg/kg, i.p.) improved it (P < 0.001). Administration of the selective 5‐HT1B/1D antagonist GR‐127935 (0.01 mg/kg, i.p.) reversed the anticonvulsive effects of sumatriptan (0.01 mg/kg, i.p.). Although both tumor necrosis factor‐α (TNF‐α) and NO levels were markedly elevated in the rats' brain tissues post‐SE induction, pre‐treatment with sumatriptan significantly reduced both TNF‐α (P < 0.05) and NO (P < 0.001) levels. Combined GR‐127935 and sumatriptan treatment inhibited these anti‐inflammatory effects of sumatriptan, whereas combined non‐specific NOS (L‐NAME) or selective neuronal NOS (7‐nitroindazole) inhibitors and sumatriptan further reduced NO levels. In conclusion, sumatriptan exerted a protective effect against the clinical manifestations and mortality rate of SE in rats which is possibly through targeting 5‐HT1B/1D receptors, neuroinflammation, and nitrergic transmission.

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“…It has been suggested that targeting NO production with nNOS inhibitors might be an excellent opportunity for selective NOS inhibition in migraine treatment, as it is strongly associated with migraine pathophysiology [37]. Also, acute administration of L-NAME, a non-specific inhibitor of NO synthase attenuated the anti-allergic effects of sumatriptan, a 5hydroxytryptamine 1B/1D (5HT1B/1D) agonist, indicating the involvement of inducible NOS in allergic inflammation [38]. When considering the numerous roles of MCs in many biological and pathological processes, the importance of NO and NOS system regulation of MC function cannot be underestimated.…”

Section: No Regulation Of Mast Cellsmentioning

confidence: 99%

Neurotransmitter and neuropeptide regulation of mast cell function: a systematic review

Shi

et al. 2020

J Neuroinflammation

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The existence of the neural control of mast cell functions has long been proposed. Mast cells (MCs) are localized in association with the peripheral nervous system (PNS) and the brain, where they are closely aligned, anatomically and functionally, with neurons and neuronal processes throughout the body. They express receptors for and are regulated by various neurotransmitters, neuropeptides, and other neuromodulators. Consequently, modulation provided by these neurotransmitters and neuromodulators allows neural control of MC functions and involvement in the pathogenesis of mast cell–related disease states. Recently, the roles of individual neurotransmitters and neuropeptides in regulating mast cell actions have been investigated extensively. This review offers a systematic review of recent advances in our understanding of the contributions of neurotransmitters and neuropeptides to mast cell activation and the pathological implications of this regulation on mast cell–related disease states, though the full extent to which such control influences health and disease is still unclear, and a complete understanding of the mechanisms underlying the control is lacking. Future validation of animal and in vitro models also is needed, which incorporates the integration of microenvironment-specific influences and the complex, multifaceted cross-talk between mast cells and various neural signals. Moreover, new biological agents directed against neurotransmitter receptors on mast cells that can be used for therapeutic intervention need to be more specific, which will reduce their ability to support inflammatory responses and enhance their potential roles in protecting against mast cell–related pathogenesis.

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Inhibition of ovalbumin-induced allergic rhinitis by sumatriptan through the nitric oxide pathway in mice

Cited by 16 publications

References 45 publications

Beyond its anti‐migraine properties, sumatriptan is an anti‐inflammatory agent: A systematic review

Beyond its anti‐migraine properties, sumatriptan is an anti‐inflammatory agent: A systematic review

Sumatriptan reduces severity of status epilepticus induced by lithium–pilocarpine through nitrergic transmission and 5‐HT_1B/D receptors in rats: A pharmacological‐based evidence

Neurotransmitter and neuropeptide regulation of mast cell function: a systematic review

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Inhibition of ovalbumin-induced allergic rhinitis by sumatriptan through the nitric oxide pathway in mice

Cited by 16 publications

References 45 publications

Beyond its anti‐migraine properties, sumatriptan is an anti‐inflammatory agent: A systematic review

Beyond its anti‐migraine properties, sumatriptan is an anti‐inflammatory agent: A systematic review

Sumatriptan reduces severity of status epilepticus induced by lithium–pilocarpine through nitrergic transmission and 5‐HT1B/D receptors in rats: A pharmacological‐based evidence

Neurotransmitter and neuropeptide regulation of mast cell function: a systematic review

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Sumatriptan reduces severity of status epilepticus induced by lithium–pilocarpine through nitrergic transmission and 5‐HT_1B/D receptors in rats: A pharmacological‐based evidence