[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.
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
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.
[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.
Kilinc, E., Dagistan, Y., Cetinkaya, A., Tore, F. (2019). 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. Clinical and Experimental Health Sciences, 9(1), 34-41. https://doi.org/10.5152/clinexphealthsci.2018.923
AMA
Kilinc E, Dagistan Y, Cetinkaya A, Tore F. 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. Clinical and Experimental Health Sciences. March 2019;9(1):34-41. doi:10.5152/clinexphealthsci.2018.923
Chicago
Kilinc, Erkan, Yasar Dagistan, Ayhan Cetinkaya, and Fatma Tore. “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”. Clinical and Experimental Health Sciences 9, no. 1 (March 2019): 34-41. https://doi.org/10.5152/clinexphealthsci.2018.923.
EndNote
Kilinc E, Dagistan Y, Cetinkaya A, Tore F (March 1, 2019) 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. Clinical and Experimental Health Sciences 9 1 34–41.
IEEE
E. Kilinc, Y. Dagistan, A. Cetinkaya, and F. Tore, “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”, Clinical and Experimental Health Sciences, vol. 9, no. 1, pp. 34–41, 2019, doi: 10.5152/clinexphealthsci.2018.923.
ISNAD
Kilinc, Erkan et al. “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”. Clinical and Experimental Health Sciences 9/1 (March 2019), 34-41. https://doi.org/10.5152/clinexphealthsci.2018.923.
JAMA
Kilinc E, Dagistan Y, Cetinkaya A, Tore F. 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. Clinical and Experimental Health Sciences. 2019;9:34–41.
MLA
Kilinc, Erkan et al. “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”. Clinical and Experimental Health Sciences, vol. 9, no. 1, 2019, pp. 34-41, doi:10.5152/clinexphealthsci.2018.923.
Vancouver
Kilinc E, Dagistan Y, Cetinkaya A, Tore F. 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. Clinical and Experimental Health Sciences. 2019;9(1):34-41.