期刊名称:International Journal of Innovative Research in Science, Engineering and Technology
印刷版ISSN:2347-6710
电子版ISSN:2319-8753
出版年度:2015
卷号:4
期号:9
页码:9092
DOI:10.15680/IJIRSET.2015.0409117
出版社:S&S Publications
摘要:While STZ has been considered as endogenous NO donor and ameliorating pancreatic β-cell functions,SNP, a conventional NO donor associated with nitrosative stress and its effects on pancreatic architecture are still notclear. In view of the above background information, present study was undertaken with the objective to investigate theeffects of endogenous (STZ) and exogenous (SNP) NO donor induced nitrosative stress on pancreatic architecture andβ-cell physiology. Swiss strain female mice, Mus musculus were divided into 3 groups- control group, STZ group (anendogenous NO donor, administered with single dose of 16 mg/100 gm body weight) and SNP group (an exogenousNO donor, administered with SNP 0.25 mg/100 gm body weight) for 7 days intraperitoneally. Results showed that NOlevel was significantly increased in both STZ and SNP treated mice accompanied with increased AGE, MDA andAOPP level in plasma as well as in pancreatic tissue. Increased intracellular ROS and Ca2+ displayed by isolatedpancreatic islets. Intense immunoreactivity for iNOS was seen in both treated groups as compared to control. However,strong immunoreactivity for insulin in the β-cells of pancreatic islets was observed in SNP treated mice which waslacking in STZ treated mice due to selective destruction of β-cells by the diabetogenic drug STZ. Morphometricresults demonstrated that pancreatic architecture as well as β-cell physiology was altered in both endogenous (STZ) andexogenous (SNP) NO donor groups. Our findings suggest that both NO donors executed their effects by causingoxidative stress (increased ROS) and islet inflammation (increased ir-iNOS). Further, exogenous NO donor provokeshyperinsulemia like condition.