Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus
Hypogonadism is a complication associated with type 1 Diabetes mellitus (DM1). Hyperglycemia and lack of insulin trigger oxidative and nitrosative stress weakening the Leydig cells, which produce testosterone. Our objective was to evaluate the effect of the flavonoid naringin (NAR) as a protector of...
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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/39047 |
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I10-R327-article-39047 |
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Universidad Nacional de Córdoba |
| institution_str |
I-10 |
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R-327 |
| container_title_str |
Revista de la Facultad de Ciencias Médicas de Córdoba |
| format |
Artículo revista |
| topic |
experimental diabetes mellitus hypogonadism antioxidant naringin diabetes mellitus experimental hipogonadismo antioxidante naringina |
| spellingShingle |
experimental diabetes mellitus hypogonadism antioxidant naringin diabetes mellitus experimental hipogonadismo antioxidante naringina Mena, C Rodríguez, V Moine, L Silvano, L Tolosa de Talamoni , N Díaz de Barboza, G Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus |
| topic_facet |
experimental diabetes mellitus hypogonadism antioxidant naringin diabetes mellitus experimental hipogonadismo antioxidante naringina |
| author |
Mena, C Rodríguez, V Moine, L Silvano, L Tolosa de Talamoni , N Díaz de Barboza, G |
| author_facet |
Mena, C Rodríguez, V Moine, L Silvano, L Tolosa de Talamoni , N Díaz de Barboza, G |
| author_sort |
Mena, C |
| title |
Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus |
| title_short |
Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus |
| title_full |
Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus |
| title_fullStr |
Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus |
| title_full_unstemmed |
Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus |
| title_sort |
protective effect of naringin in an experimental model of hypogonadism associated with type 1 diabetes mellitus |
| description |
Hypogonadism is a complication associated with type 1 Diabetes mellitus (DM1). Hyperglycemia and lack of insulin trigger oxidative and nitrosative stress weakening the Leydig cells, which produce testosterone. Our objective was to evaluate the effect of the flavonoid naringin (NAR) as a protector of Leydig cells in an experimental model of DM1.
Control male Wistar rats (C), rats treated with 60 mg streptozotocin/kg b.w. (STZ) and STZ rats treated with NAR (20, 40 or 80 mg/kg b.w., STZ+NAR) were employed. After 30 days of treatment, the rats were sacrificed and blood and testes were obtained. Blood glucose, HbA1c and serum testosterone were determined. Glutathione content (GSH) and catalase (CAT) activity were quantified in testis homogenates. In testicular sections, the expression of the inducible enzyme nitric oxide synthase (iNOS) was evaluated by immunohistochemistry and cell apoptosis by TUNEL. The results were analyzed by ANOVA/Tukey (p<0.05). The project was approved by the CICUAL from the School of Medicine, UNC (50/17).
The STZ rats exhibited increase in the serum glucose and HbA1c values. The different doses of NAR did not affect these variables. Serum testosterone levels were lower in STZ rats. NAR40 and NAR80 treatments partially prevented this decrease (C: 5.05±0.72; STZ:1.27±0.07*; STZ+NAR20:1.55±0.13*; STZ+NAR40:2.82±0.16*#; STZ+NAR80:2.56±0.36*# ng/mL, *p<0.05 vs C, #p<0.05 vs STZ and STZ+NAR20). Therefore, the chosen treatment dose was 40 mg/kg b.w. STZ rats had lower GSH content and higher CAT activity than controls. NAR normalized these parameters. The percentage of Leydig cells with positive iNOS staining was higher in diabetic rats and NAR prevented this increase (C:35.88±7.56; STZ:77.12±6.74*; STZ+NAR:28.69±8.09, *p<0.001 vs C and STZ+NAR). The number of TUNEL (+) cells was significantly increased in the STZ group. NAR treatment blocked this enhancement (C:5.83±1.13; STZ:71.07±28.36*; STZ+NAR:5.42±3.92; *p<0.05 vs C and STZ+NAR).
The results indicate that NAR prevents the cell death by apoptosis of the Leydig cells in the experimental DM1 avoiding, at least in part, the increase in the testicular oxidative and nitrosative stress. |
| 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/39047 |
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I10-R327-article-390472024-04-15T16:14:45Z Protective effect of naringin in an experimental model of hypogonadism associated with type 1 Diabetes mellitus Efecto protector de naringina en un modelo experimental de hipogonadismo asociado a Diabetes mellitus tipo 1 Mena, C Rodríguez, V Moine, L Silvano, L Tolosa de Talamoni , N Díaz de Barboza, G experimental diabetes mellitus hypogonadism antioxidant naringin diabetes mellitus experimental hipogonadismo antioxidante naringina Hypogonadism is a complication associated with type 1 Diabetes mellitus (DM1). Hyperglycemia and lack of insulin trigger oxidative and nitrosative stress weakening the Leydig cells, which produce testosterone. Our objective was to evaluate the effect of the flavonoid naringin (NAR) as a protector of Leydig cells in an experimental model of DM1. Control male Wistar rats (C), rats treated with 60 mg streptozotocin/kg b.w. (STZ) and STZ rats treated with NAR (20, 40 or 80 mg/kg b.w., STZ+NAR) were employed. After 30 days of treatment, the rats were sacrificed and blood and testes were obtained. Blood glucose, HbA1c and serum testosterone were determined. Glutathione content (GSH) and catalase (CAT) activity were quantified in testis homogenates. In testicular sections, the expression of the inducible enzyme nitric oxide synthase (iNOS) was evaluated by immunohistochemistry and cell apoptosis by TUNEL. The results were analyzed by ANOVA/Tukey (p<0.05). The project was approved by the CICUAL from the School of Medicine, UNC (50/17). The STZ rats exhibited increase in the serum glucose and HbA1c values. The different doses of NAR did not affect these variables. Serum testosterone levels were lower in STZ rats. NAR40 and NAR80 treatments partially prevented this decrease (C: 5.05±0.72; STZ:1.27±0.07*; STZ+NAR20:1.55±0.13*; STZ+NAR40:2.82±0.16*#; STZ+NAR80:2.56±0.36*# ng/mL, *p<0.05 vs C, #p<0.05 vs STZ and STZ+NAR20). Therefore, the chosen treatment dose was 40 mg/kg b.w. STZ rats had lower GSH content and higher CAT activity than controls. NAR normalized these parameters. The percentage of Leydig cells with positive iNOS staining was higher in diabetic rats and NAR prevented this increase (C:35.88±7.56; STZ:77.12±6.74*; STZ+NAR:28.69±8.09, *p<0.001 vs C and STZ+NAR). The number of TUNEL (+) cells was significantly increased in the STZ group. NAR treatment blocked this enhancement (C:5.83±1.13; STZ:71.07±28.36*; STZ+NAR:5.42±3.92; *p<0.05 vs C and STZ+NAR). The results indicate that NAR prevents the cell death by apoptosis of the Leydig cells in the experimental DM1 avoiding, at least in part, the increase in the testicular oxidative and nitrosative stress. El hipogonadismo es una complicación asociada a la Diabetes mellitus tipo 1 (DM1). La hiperglucemia y la falta de insulina desencadenan estrés oxidativo y nitrosativo afectando a las células de Leydig, productoras de testosterona. Nuestro objetivo fue evaluar el efecto del flavonoide naringina (NAR) como protector de las células de Leydig en un modelo experimental de DM1. Se emplearon ratas Wistar machos controles, tratadas con 60 mg de estreptozotocina/kg peso corporal (pc) (STZ) y ratas STZ tratadas con NAR (20, 40 u 80 mg/kg pc, STZ+NAR). A los 30 días de tratamiento, las ratas se sacrificaron y se obtuvo sangre y testículos. Se determinó glucemia, HbA1c y testosterona sérica. En homogeneizados de testículos se cuantificó el glutatión (GSH) y la actividad de catalasa (CAT). En cortes testiculares se evaluó la expresión de la enzima óxido nítrico sintasa inducible (iNOS) por inmunohistoquímica y apoptosis celular por TUNEL. Los resultados se analizaron mediante ANOVA/Tukey (p<0,05). Aprobación de CICUAL (50/17). Las ratas STZ presentaron valores de glucemia y HbA1c por encima de los valores normales. NAR no logró evitar tales efectos en ninguna de las dosis estudiadas. La testosterona sérica disminuyó en las ratas diabéticas. La administración de NAR 40 u 80 mg/kg pc logró prevenir parcialmente esta disminución (C:5,05±0,72; STZ:1,27±0,07*; STZ+NAR20:1,55±0,13*; STZ+NAR40:2,82±0,16*#; STZ+NAR80:2,56±0,36*#, ng/mL, *p<0,05 vs C, #p<0,05 vs STZ y STZ+NAR20). Por lo tanto, la dosis de tratamiento elegida fue la de 40 mg/kg pc. Las ratas STZ presentaron menor contenido de GSH y mayor actividad de CAT que las controles. NAR normalizó dichos parámetros. El porcentaje de células de Leydig con tinción de iNOS positiva fue mayor en las ratas diabéticas y NAR evitó este aumento (C:35,88±7,56; STZ:77,12±6,74*; STZ+NAR:28,69±8,09, *p<0,001 vs C y STZ+NAR). El número de células de Leydig TUNEL positivas aumentó significativamente en el grupo STZ. El tratamiento con NAR impidió este aumento (C:5,83±1,13; STZ:71,07±28,36*; STZ+NAR:5,42±3,92; *p<0,05 vs C y STZ+NAR). Los resultados indican que en la DM1 experimental NAR previene la muerte por apoptosis de las células de Leydig a través de evitar, al menos en parte, el incremento del estrés oxidativo y nitrosativo testicular. 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/39047 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 |