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Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland

Oral Diseases (2010) 16, 661–667 Objective:  To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland. Materials and methods:  Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of i...

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Published in:Oral diseases 2010-10, Vol.16 (7), p.661-667
Main Authors: Çevik-Aras, H, Ekström, J
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description Oral Diseases (2010) 16, 661–667 Objective:  To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland. Materials and methods:  Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration. Results:  The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response. Conclusion:  Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.
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Materials and methods:  Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration. Results:  The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response. Conclusion:  Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.</description><identifier>ISSN: 1354-523X</identifier><identifier>EISSN: 1601-0825</identifier><identifier>DOI: 10.1111/j.1601-0825.2010.01672.x</identifier><identifier>PMID: 20846152</identifier><language>eng</language><publisher>Oxford, UK: Blackwell Publishing Ltd</publisher><subject><![CDATA[Animals ; anti-inflammatory ; Anti-Inflammatory Agents - administration & dosage ; Anti-Inflammatory Agents - therapeutic use ; cholecystokinin ; Dentistry ; dysfunction ; Escherichia coli ; Hormone Antagonists - pharmacology ; inflammation ; Injections, Intraperitoneal ; lipopolysaccharide ; lipopolysaccharide-induced salivary gland inflammation ; Lipopolysaccharides - adverse effects ; Lysine - analogs & derivatives ; Lysine - pharmacology ; melatonin ; Melatonin - administration & dosage ; Melatonin - antagonists & inhibitors ; Melatonin - therapeutic use ; myeloperoxidase ; myeloperoxidase activity ; neutrophil content ; Neutrophil Infiltration - drug effects ; NG-Nitroarginine Methyl Ester - pharmacology ; Nitric Oxide Synthase - antagonists & inhibitors ; Nitric Oxide Synthase Type I - antagonists & inhibitors ; Nitric Oxide Synthase Type II - antagonists & inhibitors ; nitric oxide-synthase inhibitors ; nitric-oxide ; Odontologi ; Organ Size ; oxidative stress ; Parasympathectomy ; Parotid Gland - drug effects ; Parotid Gland - enzymology ; Parotid Gland - innervation ; Parotitis - chemically induced ; Parotitis - enzymology ; Parotitis - prevention & control ; Peroxidase - analysis ; Proglumide - analogs & derivatives ; Proglumide - pharmacology ; prostaglandins ; Rats ; Rats, Sprague-Dawley ; Receptor, Cholecystokinin A - antagonists & inhibitors ; Receptor, Melatonin, MT2 - antagonists & inhibitors ; salivary ; secretion ; Sincalide - administration & dosage ; Sincalide - antagonists & inhibitors ; Sincalide - therapeutic use ; Sympathectomy ; Tryptamines - pharmacology]]></subject><ispartof>Oral diseases, 2010-10, Vol.16 (7), p.661-667</ispartof><rights>2010 John Wiley &amp; Sons A/S</rights><rights>2010 John Wiley &amp; Sons A/S.</rights><lds50>peer_reviewed</lds50><woscitedreferencessubscribed>false</woscitedreferencessubscribed><citedby>FETCH-LOGICAL-c4612-d2ea4e9c253a66868968068bda2d7d780db533e745f450ac4c1bd4df982215893</citedby></display><links><openurl>$$Topenurl_article</openurl><openurlfulltext>$$Topenurlfull_article</openurlfulltext><thumbnail>$$Tsyndetics_thumb_exl</thumbnail><link.rule.ids>230,314,780,784,885,27924,27925</link.rule.ids><backlink>$$Uhttps://www.ncbi.nlm.nih.gov/pubmed/20846152$$D View this record in MEDLINE/PubMed$$Hfree_for_read</backlink><backlink>$$Uhttps://gup.ub.gu.se/publication/139412$$DView record from Swedish Publication Index$$Hfree_for_read</backlink></links><search><creatorcontrib>Çevik-Aras, H</creatorcontrib><creatorcontrib>Ekström, J</creatorcontrib><title>Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland</title><title>Oral diseases</title><addtitle>Oral Dis</addtitle><description>Oral Diseases (2010) 16, 661–667 Objective:  To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland. Materials and methods:  Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration. Results:  The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response. Conclusion:  Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.</description><subject>Animals</subject><subject>anti-inflammatory</subject><subject>Anti-Inflammatory Agents - administration &amp; dosage</subject><subject>Anti-Inflammatory Agents - therapeutic use</subject><subject>cholecystokinin</subject><subject>Dentistry</subject><subject>dysfunction</subject><subject>Escherichia coli</subject><subject>Hormone Antagonists - pharmacology</subject><subject>inflammation</subject><subject>Injections, Intraperitoneal</subject><subject>lipopolysaccharide</subject><subject>lipopolysaccharide-induced salivary gland inflammation</subject><subject>Lipopolysaccharides - adverse effects</subject><subject>Lysine - analogs &amp; derivatives</subject><subject>Lysine - pharmacology</subject><subject>melatonin</subject><subject>Melatonin - administration &amp; dosage</subject><subject>Melatonin - antagonists &amp; inhibitors</subject><subject>Melatonin - therapeutic use</subject><subject>myeloperoxidase</subject><subject>myeloperoxidase activity</subject><subject>neutrophil content</subject><subject>Neutrophil Infiltration - drug effects</subject><subject>NG-Nitroarginine Methyl Ester - pharmacology</subject><subject>Nitric Oxide Synthase - antagonists &amp; inhibitors</subject><subject>Nitric Oxide Synthase Type I - antagonists &amp; inhibitors</subject><subject>Nitric Oxide Synthase Type II - antagonists &amp; inhibitors</subject><subject>nitric oxide-synthase inhibitors</subject><subject>nitric-oxide</subject><subject>Odontologi</subject><subject>Organ Size</subject><subject>oxidative stress</subject><subject>Parasympathectomy</subject><subject>Parotid Gland - drug effects</subject><subject>Parotid Gland - enzymology</subject><subject>Parotid Gland - innervation</subject><subject>Parotitis - chemically induced</subject><subject>Parotitis - enzymology</subject><subject>Parotitis - prevention &amp; control</subject><subject>Peroxidase - analysis</subject><subject>Proglumide - analogs &amp; derivatives</subject><subject>Proglumide - pharmacology</subject><subject>prostaglandins</subject><subject>Rats</subject><subject>Rats, Sprague-Dawley</subject><subject>Receptor, Cholecystokinin A - antagonists &amp; inhibitors</subject><subject>Receptor, Melatonin, MT2 - antagonists &amp; inhibitors</subject><subject>salivary</subject><subject>secretion</subject><subject>Sincalide - administration &amp; dosage</subject><subject>Sincalide - antagonists &amp; inhibitors</subject><subject>Sincalide - therapeutic use</subject><subject>Sympathectomy</subject><subject>Tryptamines - pharmacology</subject><issn>1354-523X</issn><issn>1601-0825</issn><fulltext>true</fulltext><rsrctype>article</rsrctype><creationdate>2010</creationdate><recordtype>article</recordtype><recordid>eNpFkU1v1DAQhi0Eoh_wF5BvnLL4O86BQynQVipUQkXlNnJiZ-ttEqexo-7--zpsWayRPJ55ZjyaFyFMyYrm82mzoorQgmgmV4zkKKGqZKvtK3R8SLzOPpeikIz_OUInMW4IoWXF2Vt0xIgWikp2jH6dDckXfmg70_cmhWmHTZN8GHBocXMfOtfsYgoPfvADNoPFvesytryypXuHJ5PwaKaQvMXrLiPv0JvWdNG9f7lP0e_v327PL4vrm4ur87Prosl_s8IyZ4SrGia5UUorXSlNlK6tYba0pSa2lpy7UshWSGIa0dDaCttWmjEqdcVPUbHvG5_cONcwTr430w6C8bCeR8ih9QzRAeWVoCzzH_f8OIXH2cUEvY-N6_LMLswRSilpSUW1kB9eyLnunT10_re2DHzeA0--c7tDnhJY5IENLCrAogIs8sBfeWALN1-vFu__6D4mtz3Um-kBVMlLCXc_L-CH_MLV5d0tKP4M_hySUQ</recordid><startdate>201010</startdate><enddate>201010</enddate><creator>Çevik-Aras, H</creator><creator>Ekström, J</creator><general>Blackwell Publishing Ltd</general><scope>BSCLL</scope><scope>CGR</scope><scope>CUY</scope><scope>CVF</scope><scope>ECM</scope><scope>EIF</scope><scope>NPM</scope><scope>7X8</scope><scope>ADTPV</scope><scope>AOWAS</scope><scope>F1U</scope></search><sort><creationdate>201010</creationdate><title>Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland</title><author>Çevik-Aras, H ; Ekström, J</author></sort><facets><frbrtype>5</frbrtype><frbrgroupid>cdi_FETCH-LOGICAL-c4612-d2ea4e9c253a66868968068bda2d7d780db533e745f450ac4c1bd4df982215893</frbrgroupid><rsrctype>articles</rsrctype><prefilter>articles</prefilter><language>eng</language><creationdate>2010</creationdate><topic>Animals</topic><topic>anti-inflammatory</topic><topic>Anti-Inflammatory Agents - administration &amp; dosage</topic><topic>Anti-Inflammatory Agents - therapeutic use</topic><topic>cholecystokinin</topic><topic>Dentistry</topic><topic>dysfunction</topic><topic>Escherichia coli</topic><topic>Hormone Antagonists - pharmacology</topic><topic>inflammation</topic><topic>Injections, Intraperitoneal</topic><topic>lipopolysaccharide</topic><topic>lipopolysaccharide-induced salivary gland inflammation</topic><topic>Lipopolysaccharides - adverse effects</topic><topic>Lysine - analogs &amp; derivatives</topic><topic>Lysine - pharmacology</topic><topic>melatonin</topic><topic>Melatonin - administration &amp; dosage</topic><topic>Melatonin - antagonists &amp; inhibitors</topic><topic>Melatonin - therapeutic use</topic><topic>myeloperoxidase</topic><topic>myeloperoxidase activity</topic><topic>neutrophil content</topic><topic>Neutrophil Infiltration - drug effects</topic><topic>NG-Nitroarginine Methyl Ester - pharmacology</topic><topic>Nitric Oxide Synthase - antagonists &amp; inhibitors</topic><topic>Nitric Oxide Synthase Type I - antagonists &amp; inhibitors</topic><topic>Nitric Oxide Synthase Type II - antagonists &amp; inhibitors</topic><topic>nitric oxide-synthase inhibitors</topic><topic>nitric-oxide</topic><topic>Odontologi</topic><topic>Organ Size</topic><topic>oxidative stress</topic><topic>Parasympathectomy</topic><topic>Parotid Gland - drug effects</topic><topic>Parotid Gland - enzymology</topic><topic>Parotid Gland - innervation</topic><topic>Parotitis - chemically induced</topic><topic>Parotitis - enzymology</topic><topic>Parotitis - prevention &amp; control</topic><topic>Peroxidase - analysis</topic><topic>Proglumide - analogs &amp; derivatives</topic><topic>Proglumide - pharmacology</topic><topic>prostaglandins</topic><topic>Rats</topic><topic>Rats, Sprague-Dawley</topic><topic>Receptor, Cholecystokinin A - antagonists &amp; inhibitors</topic><topic>Receptor, Melatonin, MT2 - antagonists &amp; inhibitors</topic><topic>salivary</topic><topic>secretion</topic><topic>Sincalide - administration &amp; dosage</topic><topic>Sincalide - antagonists &amp; inhibitors</topic><topic>Sincalide - therapeutic use</topic><topic>Sympathectomy</topic><topic>Tryptamines - pharmacology</topic><toplevel>peer_reviewed</toplevel><toplevel>online_resources</toplevel><creatorcontrib>Çevik-Aras, H</creatorcontrib><creatorcontrib>Ekström, J</creatorcontrib><collection>Istex</collection><collection>Medline</collection><collection>MEDLINE</collection><collection>MEDLINE (Ovid)</collection><collection>MEDLINE</collection><collection>MEDLINE</collection><collection>PubMed</collection><collection>MEDLINE - Academic</collection><collection>SwePub</collection><collection>SwePub Articles</collection><collection>SWEPUB Göteborgs universitet</collection><jtitle>Oral diseases</jtitle></facets><delivery><delcategory>Remote Search Resource</delcategory><fulltext>fulltext</fulltext></delivery><addata><au>Çevik-Aras, H</au><au>Ekström, J</au><format>journal</format><genre>article</genre><ristype>JOUR</ristype><atitle>Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland</atitle><jtitle>Oral diseases</jtitle><addtitle>Oral Dis</addtitle><date>2010-10</date><risdate>2010</risdate><volume>16</volume><issue>7</issue><spage>661</spage><epage>667</epage><pages>661-667</pages><issn>1354-523X</issn><eissn>1601-0825</eissn><abstract>Oral Diseases (2010) 16, 661–667 Objective:  To define the influence of cholecystokinin and melatonin on the inflammatory response of the lipopolysaccharide‐exposed rat parotid gland. Materials and methods:  Bacterial lipopolysaccharide was infused retrogradely into the parotid duct. The degree of inflammation three hours postadministration was estimated from the activity of myeloperoxidase, reflecting glandular neutrophil infiltration. Results:  The myeloperoxidase activity of the lipopolysaccharide‐exposed gland was 10‐fold greater than that of the contralateral gland. Combined with sulphated cholecystokinin‐8 (10 or 25 μg kg−1, given twice intraperitoneally) or melatonin (10 or 25 mg kg−1 × 2) the lipopolysaccharide‐induced response was elevated 4.6‐ and 3.5‐folds at the most. The cholecystokinin‐A receptor antagonist lorglumide reduced the inhibitory effect of cholecystokinin‐8, while the melatonin 2‐preferring receptor antagonist luzindole had no effect on the melatonin‐induced inhibition. Unselective nitric oxide‐synthase inhibition abolished the increase in myeloperoxidase activity, whereas inhibition of inducible or neuronal nitric oxide‐synthase (of non‐nervous origin) halved the inflammatory response. Conclusion:  Some hormones may contribute to anti‐inflammatory action in salivary glands in physiological conditions. They are potential pharmacological tools for treating gland inflammation. The inflammation, as judged from the myeloperoxidase activity, was entirely dependent on nitric oxide‐synthase activity, indicating that the hormones directly or indirectly reduced the generation of nitric oxide.</abstract><cop>Oxford, UK</cop><pub>Blackwell Publishing Ltd</pub><pmid>20846152</pmid><doi>10.1111/j.1601-0825.2010.01672.x</doi><tpages>7</tpages></addata></record>
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subjects Animals
anti-inflammatory
Anti-Inflammatory Agents - administration & dosage
Anti-Inflammatory Agents - therapeutic use
cholecystokinin
Dentistry
dysfunction
Escherichia coli
Hormone Antagonists - pharmacology
inflammation
Injections, Intraperitoneal
lipopolysaccharide
lipopolysaccharide-induced salivary gland inflammation
Lipopolysaccharides - adverse effects
Lysine - analogs & derivatives
Lysine - pharmacology
melatonin
Melatonin - administration & dosage
Melatonin - antagonists & inhibitors
Melatonin - therapeutic use
myeloperoxidase
myeloperoxidase activity
neutrophil content
Neutrophil Infiltration - drug effects
NG-Nitroarginine Methyl Ester - pharmacology
Nitric Oxide Synthase - antagonists & inhibitors
Nitric Oxide Synthase Type I - antagonists & inhibitors
Nitric Oxide Synthase Type II - antagonists & inhibitors
nitric oxide-synthase inhibitors
nitric-oxide
Odontologi
Organ Size
oxidative stress
Parasympathectomy
Parotid Gland - drug effects
Parotid Gland - enzymology
Parotid Gland - innervation
Parotitis - chemically induced
Parotitis - enzymology
Parotitis - prevention & control
Peroxidase - analysis
Proglumide - analogs & derivatives
Proglumide - pharmacology
prostaglandins
Rats
Rats, Sprague-Dawley
Receptor, Cholecystokinin A - antagonists & inhibitors
Receptor, Melatonin, MT2 - antagonists & inhibitors
salivary
secretion
Sincalide - administration & dosage
Sincalide - antagonists & inhibitors
Sincalide - therapeutic use
Sympathectomy
Tryptamines - pharmacology
title Anti-inflammatory action of cholecystokinin and melatonin in the rat parotid gland
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