Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits
2015
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ObjectivesThe influence of experimental diabetes (alloxan, 100mgkg(-1))
was studied on rabbit parotid gland function.
Material and MethodsCarbachol-induced parotid secretion in vivo, and in
vitro quantification of inducible nitric oxide synthase (iNOS) mRNA
expression, by real-time RT-PCR, and activity of superoxide dismutase
(SOD) and total antioxidant capacity (TAC) in commercial colorimetric
assays were measured in parotid glands of non-diabetic and diabetic
rabbits.
ResultsCarbachol-induced dose-dependent increase in parotid secretion
significantly reduced in diabetic rabbits. Functional studies in the
presence of muscarinic receptor and nitric oxide synthase (NOS)
antagonists revealed that in M-3 receptor-mediated carbachol secretion,
nitric oxide, deriving mainly from neuronal NOS (nNOS) in control, and
iNOS in diabetic rabbits, was involved. Also, upregulation of iNOS mRNA
expression and enhanced SOD activity and TAC were detected in diabetic
glands.
ConclusionsOur data suggest that decreased M-3 receptor-mediated parotid
secretion in diabetic rabbits appears to be due to alterations in NO
signaling, mainly due to iNOS induction, accompanied by elevated
antioxidant response.
Кључне речи:
diabetes; parotid secretion; inducible nitric oxide synthase; oxidative stressИзвор:
Oral Diseases, 2015, 21, 5, 634-640
DOI: 10.1111/odi.12327
ISSN: 1601-0825