Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin
Diabetes mellitus (DM) is a risk factor for the development of systemic atherosclerosis and vascular calcification (VC). Chronic inflammation and oxidative stress might be the involved mechanisms in the VC. Hyperglycemia produces oxygen- and nitrogen-derived free radicals (ROS) and triggers endothel...
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Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología
2022
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| Acceso en línea: | https://revistas.unc.edu.ar/index.php/med/article/view/39067 |
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I10-R327-article-39067 |
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ojs |
| institution |
Universidad Nacional de Córdoba |
| institution_str |
I-10 |
| repository_str |
R-327 |
| container_title_str |
Revista de la Facultad de Ciencias Médicas de Córdoba |
| format |
Artículo revista |
| topic |
diabetes mellitus vascular calcification nitric oxide diabetes mellitus calcificación vascular óxido nítrico |
| spellingShingle |
diabetes mellitus vascular calcification nitric oxide diabetes mellitus calcificación vascular óxido nítrico Baulies, D Campelo, A Massheimer , V Tolosa de Talamoni , N Rivoira , MA Díaz de Barboza, G Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin |
| topic_facet |
diabetes mellitus vascular calcification nitric oxide diabetes mellitus calcificación vascular óxido nítrico |
| author |
Baulies, D Campelo, A Massheimer , V Tolosa de Talamoni , N Rivoira , MA Díaz de Barboza, G |
| author_facet |
Baulies, D Campelo, A Massheimer , V Tolosa de Talamoni , N Rivoira , MA Díaz de Barboza, G |
| author_sort |
Baulies, D |
| title |
Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin |
| title_short |
Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin |
| title_full |
Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin |
| title_fullStr |
Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin |
| title_full_unstemmed |
Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin |
| title_sort |
arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin |
| description |
Diabetes mellitus (DM) is a risk factor for the development of systemic atherosclerosis and vascular calcification (VC). Chronic inflammation and oxidative stress might be the involved mechanisms in the VC. Hyperglycemia produces oxygen- and nitrogen-derived free radicals (ROS) and triggers endothelial cell (EC) dysfunction. Treatment with natural antioxidants is likely to prevent these complications. Aim: To evaluate the effect of Naringin (NAR) as a CV protector in an experimental model of type 1 DM.
Wistar rats were divided in controls (C), diabetic (STZ, treated with 60 mg of streptozotocin/kg b.w.) and diabetic treated with NAR (40 mg/kg b.w.). CICUAL:16/08/2018. The animals were sacrificed 30 days post-treatment after blood extraction and the aortas were obtained. Serum alkaline phosphatase (AP) activity and ROS level in red blood cells were determined. In histological sections of aorta, the morphology of the vascular wall was analyzed with H&E. In cultured aortic ECs, the NO• content, an indicator of vascular health, and the expression of the enzyme inducible nitric oxide synthase (iNOS) were quantified by immunohistochemistry. ANOVA and Tukey were used for statistical analysis (p<0.05).
AP activity and ROS level increased in STZ rats and returned to control values with NAR (AP: C:198.50±28.78; STZ:515.20±54.23*; NAR:227.80±46.43 IU/L; *p<0.001vs C and NAR. ROS: C:224.66±1.45; STZ:327.33±41.28*; NAR:218.33±17.37 AU; *p<0.05 vs C and NAR). NO• content and iNOS expression in ECs from diabetic rats decreased by 33 and 25%, respectively. NAR only normalized NO• values. Aortas from all groups were exposed to procalcifying medium for 7 days, then decalcified and the released calcium was quantified spectrophotometrically. Calcium content was higher in STZ rats and NAR normalized the values (C:8.7±0.5; STZ:15.1±0.8*; NAR:10.8±0.7 mg Ca2+/dL; *p<0.01 vs C and NAR). NAR partially prevented the decrease in aortas muscle fiber width in STZ group.
These results demonstrate that NAR improves vascular health, attenuates CV and restores NO• levels in a diabetes mellitus experimental model. |
| publisher |
Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología |
| publishDate |
2022 |
| url |
https://revistas.unc.edu.ar/index.php/med/article/view/39067 |
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2024-09-03T21:04:06Z |
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2024-09-03T21:04:06Z |
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I10-R327-article-390672024-04-15T16:14:45Z Arterial disfunction associated to experimental type 1 diabetes mellitus, protective effect of naringin Disfunción arterial asociada a la diabetes mellitus tipo 1 experimental, efecto protector de naringina Baulies, D Campelo, A Massheimer , V Tolosa de Talamoni , N Rivoira , MA Díaz de Barboza, G diabetes mellitus vascular calcification nitric oxide diabetes mellitus calcificación vascular óxido nítrico Diabetes mellitus (DM) is a risk factor for the development of systemic atherosclerosis and vascular calcification (VC). Chronic inflammation and oxidative stress might be the involved mechanisms in the VC. Hyperglycemia produces oxygen- and nitrogen-derived free radicals (ROS) and triggers endothelial cell (EC) dysfunction. Treatment with natural antioxidants is likely to prevent these complications. Aim: To evaluate the effect of Naringin (NAR) as a CV protector in an experimental model of type 1 DM. Wistar rats were divided in controls (C), diabetic (STZ, treated with 60 mg of streptozotocin/kg b.w.) and diabetic treated with NAR (40 mg/kg b.w.). CICUAL:16/08/2018. The animals were sacrificed 30 days post-treatment after blood extraction and the aortas were obtained. Serum alkaline phosphatase (AP) activity and ROS level in red blood cells were determined. In histological sections of aorta, the morphology of the vascular wall was analyzed with H&E. In cultured aortic ECs, the NO• content, an indicator of vascular health, and the expression of the enzyme inducible nitric oxide synthase (iNOS) were quantified by immunohistochemistry. ANOVA and Tukey were used for statistical analysis (p<0.05). AP activity and ROS level increased in STZ rats and returned to control values with NAR (AP: C:198.50±28.78; STZ:515.20±54.23*; NAR:227.80±46.43 IU/L; *p<0.001vs C and NAR. ROS: C:224.66±1.45; STZ:327.33±41.28*; NAR:218.33±17.37 AU; *p<0.05 vs C and NAR). NO• content and iNOS expression in ECs from diabetic rats decreased by 33 and 25%, respectively. NAR only normalized NO• values. Aortas from all groups were exposed to procalcifying medium for 7 days, then decalcified and the released calcium was quantified spectrophotometrically. Calcium content was higher in STZ rats and NAR normalized the values (C:8.7±0.5; STZ:15.1±0.8*; NAR:10.8±0.7 mg Ca2+/dL; *p<0.01 vs C and NAR). NAR partially prevented the decrease in aortas muscle fiber width in STZ group. These results demonstrate that NAR improves vascular health, attenuates CV and restores NO• levels in a diabetes mellitus experimental model. La Diabetes mellitus (DM) es un factor de riesgo para el desarrollo de ateroesclerosis sistémica y calcificación vascular (CV). La inflamación crónica y el estrés oxidativo pueden ser los mecanismos implicados en la CV. La hiperglucemia produce radicales libres derivados del oxígeno (ROS) y del nitrógeno y desencadena disfunción de células endoteliales (CE). Es probable que el tratamiento con antioxidantes naturales evite estas complicaciones. Objetivo: evaluar el efecto de Naringina (NAR) como protector de las CV en un modelo experimental de DM tipo 1. Ratas Wistar se dividieron en controles (C), diabéticas (STZ, tratadas con 60 mg de estreptozotocina/kg de pc) y diabéticas tratadas con NAR (40 mg/kg pc), (CICUAL:16/08/2018). Los animales se sacrificaron 30 días post tratamiento previa extracción sanguínea y se obtuvieron las aortas. Se determinó actividad de fosfatasa alcalina sérica (FA) y nivel de ROS en glóbulos rojos. En secciones histológicas de aorta se analizó la morfología de la pared vascular con H/E. En cultivo de CE de aortas se cuantificó el contenido de NO•, indicador de salud vascular, y la expresión de la enzima óxido nítrico sintasa inducible (iNOS) por inmunohistoquímica. Se empleó ANOVA y Tukey para análisis estadístico, considerando significativo p<0,05. La actividad de FA y el nivel de ROS aumentaron en ratas STZ y retornaron a valores controles con NAR (FA: C:198,50±28,78; STZ:515,20±54,23*; NAR:227,80±46,43, UI/L; *p<0,001vs C y NAR. ROS: C:224,66±1,45; STZ:327,33±41,28*; NAR:218,33±17,37 UA; *p<0,05 vs C y NAR). El contenido de NO• y la expresión de iNOS en CE de ratas diabéticas disminuyeron un 33 y 25%, respectivamente. NAR sólo normalizó los valores de NO•. Las aortas de todos los grupos se expusieron a un medio procalcificante durante 7 días, luego se descalcificaron y el calcio liberado se cuantificó por espectrofotometría. El contenido de calcio fue mayor en ratas STZ y NAR normalizó los valores (C:8,7±0,5; STZ:15,1±0,8*; NAR:10,8±0,7 mg Ca+2/dL; *p<0,01 vs C y NAR). NAR evitó parcialmente la disminución del ancho de las fibras musculares de aortas del grupo STZ. Estos resultados demuestran que NAR mejora la salud vascular, atenúa la CV y restaura los niveles de NO• en un modelo experimental de diabetes. Universidad Nacional Córdoba. Facultad de Ciencias Médicas. Secretaria de Ciencia y Tecnología 2022-10-26 info:eu-repo/semantics/article info:eu-repo/semantics/publishedVersion texto texto texto https://revistas.unc.edu.ar/index.php/med/article/view/39067 Revista de la Facultad de Ciencias Médicas de Córdoba.; Vol. 79 No. Suplemento JIC XXIII (2022): Suplemento JIC XXIII Revista de la Facultad de Ciencias Médicas de Córdoba; Vol. 79 Núm. Suplemento JIC XXIII (2022): Suplemento JIC XXIII Revista da Faculdade de Ciências Médicas de Córdoba; v. 79 n. Suplemento JIC XXIII (2022): Suplemento JIC XXIII 1853-0605 0014-6722 http://creativecommons.org/licenses/by-nc/4.0 |