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.
TY - JOUR
AU - Roganović, Jelena
AU - Đukić, Ljiljana
AU - Kršljak, Elena
AU - Tanić, Nasta
AU - Stojić, Dragica
PY - 2015
UR - https://smile.stomf.bg.ac.rs/handle/123456789/1963
AB - 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.
PB - Wiley, Hoboken
T2 - Oral Diseases
T1 - Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits
VL - 21
IS - 5
SP - 634
EP - 640
DO - 10.1111/odi.12327
ER -
@article{
author = "Roganović, Jelena and Đukić, Ljiljana and Kršljak, Elena and Tanić, Nasta and Stojić, Dragica",
year = "2015",
abstract = "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.",
publisher = "Wiley, Hoboken",
journal = "Oral Diseases",
title = "Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits",
volume = "21",
number = "5",
pages = "634-640",
doi = "10.1111/odi.12327"
}
Roganović, J., Đukić, L., Kršljak, E., Tanić, N.,& Stojić, D.. (2015). Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits. in Oral Diseases
Wiley, Hoboken., 21(5), 634-640.
https://doi.org/10.1111/odi.12327
Roganović J, Đukić L, Kršljak E, Tanić N, Stojić D. Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits. in Oral Diseases. 2015;21(5):634-640.
doi:10.1111/odi.12327 .
Roganović, Jelena, Đukić, Ljiljana, Kršljak, Elena, Tanić, Nasta, Stojić, Dragica, "Reduced muscarinic parotid secretion is underlain by impaired NO signaling in diabetic rabbits" in Oral Diseases, 21, no. 5 (2015):634-640,
https://doi.org/10.1111/odi.12327 . .
