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 Painin

Yıl 2019, Cilt: 9 Sayı: 1, 34 - 41, 29.03.2019

Erkan Kilinc , Yasar Dagistan Ayhan Cetinkaya Fatma Tore

https://doi.org/10.5152/clinexphealthsci.2018.923

Cited By: 1

Öz

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.

Anahtar Kelimeler

Inflammatory pain, mast cell degranulation, substance-P, compound-48/80.

Kaynakça

• [1] Schlereth T, Birklein F. Mast cells: source of inflammation in complex regional pain syndrome? Anesthesiol. 2012; 116:756-7.
• [2] Theoharides TC, Alysandratos KD, Angelidou A, Delivanis DA, Sismanopoulos N, Zhang B, Asadi S, Vasiadi M, Weng Z, Miniati A, Kalogeromitros D. Mast cells and inflammation. Biochim. Biophys. Acta 2012; 1822:21-33.
• [3] Sismanopoulos N, Delivanis DA, Alysandratos KD, Angelidou A, Therianou A, Kalogeromitros D, Theoharides TC. Mast cells in allergic and inflammatory diseases. Curr. Pharm. Des. 2012;18:2261-2277.
• [4] Kilinc E, Dagistan Y, Kukner A, Yilmaz B, Agus S, Soyler G, Tore F. Salmon calcitonin ameliorates migraine pain through modulation of CGRP release and dural mast cell degranulation in rats. Clin. Exp. Pharmacol. Physiol. 2018; 45(6):536-546.
• [5] Kilinc E, Dagistan Y, Tore F. Mast cell degranulation mediates compound 48/80-induced meningeal vasodilatation underlying migraine pain. Clin. Exp. Health Sci. 2017; 196-201.
• [6] Aich A, Afrin LB, Gupta K. Mast cell-mediated mechanisms of nociception. Int. J. Mol. Sci. 2015;16:29069-29092.
• [7] Héron A, Dubayle D. A focus on mast cells and pain. J. Neuroimmunol. 2013;264:1-7.
• [8] Manchanda RK, Jaggi AS, Singh N. Ameliorative potential of sodium cromoglycate and diethyldithiocarbamic acid in restraint stress-induced behavioral alterations in rats. Pharmacol. Rep. 2011;63:54-63.
• [9] Finn DF, Walsh JJ. Twenty-first century mast cell stabilizers. Br. J. Pharmacol.2013;170:23-37.
• [10] da Silva EZ, Jamur MC, Oliver C. Mast cell function: a new vision of an old cell. J. Histochem. Cytochem. 2014;62:698-738.
• [11] Bozic CR, Lu B, Höpken UE, Gerard C, Gerard NP. Neurogenic amplification of immune complex inflammation. Science 1996;273:1722-5.
• [12] Lisowska B, Lisowski A, Siewruk K. Substance P and chronic pain in patients with chronic inflammation of connective tissue. PLoS One 2015;10:e0139206.
• [13] Straub RH, Cutolo M. Involvement of the hypothalamicpituitary- adrenal/gonadal axis and the peripheral nervous system in rheumatoid arthritis: viewpoint based on a systemic pathogenetic role. Arthritis Rheum. 2001;44:493-507.
• [14] Clay F, Morris C. British inflammation research association meeting: is there any point in developing an anti-RA drug? National Heart and Lung Institute, London, UK, 21-22 November 1996. Inflamm. Res. 1997;46:243-245.
• [15] Gabrielian L, Helps SC, Thornton E, Turner RJ, Leonard AV, Vink R. Substance P antagonists as a novel intervention for brain edema and raised intracranial pressure. Acta Neurochir. Suppl. 2013;118:201-204.
• [16] Zhang RX, Ren K. Animal models of inflammatory pain. Ma C., Zhang JM, editors. Animal models of pain. Totowa, NJ: Humana Press; 2011. p.23-41.
• [17] Levy D, Burstein R, Kainz V, Jakubowski M, Strassman AM. Mast cell degranulation activates a pain pathway underlying migraine headache. Pain 2007;130:166-176.
• [18] Sand E, Themner-Persson A, Ekblad E. Mast cells reduce survival of myenteric neurons in culture. Neuropharmacol. 2009;56:522-530.
• [19] Kilinc E, Dagistan Y, Kotan B, Cetinkaya A. Effects of Nigella sativa seeds and certain species of fungi extracts on number and activation of dural mast cells in rats. Physiol. Int. 2017;104:15-24.
• [20] Chakraborty S, Kar N, Kumari L, De A, Bera T. Inhibitory effect of a new orally active cedrol-loaded nanostructured lipid carrier on compound 48/80-induced mast cell degranulation and anaphylactic shock in mice. Int. J. Nanomedicine 2017;12:4849-4868.
• [21] Dong H, Zhang X, Wang Y, Zhou X, Qian Y, Zhang S. Suppression of Brain Mast Cells Degranulation Inhibits Microglial Activation and Central Nervous System Inflammation. Mol. Neurobiol. 2017;54:997-1007.
• [22] Kilinc E, Guerrero-Toro C, Zakharov A, Vitale C, Gubert-Olive M, Koroleva K, Timonina A, Luz LL, Shelukhina I, Giniatullina R, Tore F, Safronov BV, Giniatullin R. Serotonergic mechanisms of trigeminal meningeal nociception: Implications for migraine pain. Neuropharmacol. 2017;116:160-173.
• [23] Ferrari LF, Levine JD, Green PG. Mechanisms mediating nitroglycerin-induced delayed-onset hyperalgesia in the rat. Neurosci. 2016;317:121-129.
• [24] Kaur G, Singh N, Jaggi AS. Mast cells in neuropathic pain: an increasing spectrum of their involvement in pathophysiology. Rev. Neurosci. 2017;28:759-766.
• [25] O’Connor TM, O’Connell J, O’Brien DI, Goode T, Bredin CP, Shanahan F. The role of substance P in inflammatory disease. J. Cell Physiol. 2004;201:167-180.
• [26] Kilinc E, Firat T, Tore F, Kiyan A, Kukner A, Tunçel N. Vasoactive Intestinal peptide modulates c-Fos activity in the trigeminal nucleus and dura mater mast cells in sympathectomized rats. J. Neurosci. Res. 2015;93:644-650.
• [27] Menkes CJ, Renoux M, Laoussadi S, Mauborgne A, Bruxelle J, Cesselin F. Substance P levels in the synovium and synovial fluid from patients with rheumatoid arthritis and osteoarthritis. J. Rheumatol. 1993;20:714-717.
• [28] Tavano F, di Mola FF, Latiano A, Palmieri O, Bossa F, Valvano MR, Latiano T, Annese V, Andriulli A, di Sebastiano P. Neuroimmune interactions in patients with inflammatory bowel diseases: disease activity and clinical behavior based on Substance P serum levels. J. Crohns Colitis 2012;6:563-70.
• [29] Vincent L, Vang D, Nguyen J, Gupta M, Luk K, Ericson ME, Simone DA, Gupta K. Mast cell activation contributes to sickle cell pathobiology and pain in mice. Blood 2013; 122:1853-62. [30] Waeber C, Moskowitz MA. Migraine as an inflammatory disorder. Neurology 2005;64:S9-15.
• [31] Peroutka SJ. Neurogenic inflammation and migraine: implications for the therapeutics. Mol.Interv. 2005;5:304-11. [32] Strassman AM, Raymond SA, Burstein R. Sensitization of meningeal sensory neurons and the origin of headaches. Nature 1996; 384:560-4.
• [33] Burstein R, Yamamura H, Malick A, Strassman AM. Chemical stimulation of the intracranial dura induces enhanced responses to facial stimulation in brain stem trigeminal neurons. J. Neurophysiol. 1998;79:964-82.