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

• Published in: Oral diseases 2010-10, Vol.16 (7), p.661-667
• Main Authors: Çevik-Aras, H, Ekström, J
• Format: Article
• Language: English
• 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
• ISSN: 1354-523X; 1601-0825
• DOI: 10.1111/j.1601-0825.2010.01672.x

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.