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1.
Phytomedicine ; 123: 155217, 2024 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-37992492

RESUMO

BACKGROUND: Owing to the early suffering age and the rising incidence of type 1 diabetes (T1D), the resulting male reproductive dysfunction and fertility decline have become a disturbing reality worldwide, with no effective strategy being available. Icariin (ICA), a flavonoid extracted from Herba Epimedium, has been proved its promising application in improving diabetes-related complications including diabetic nephropathy, endothelial dysfunction and erectile dysfunction. Ensuring the future reproductive health of children and adolescents with T1D is crucial to improve global fertility. However, its roles in the treatment of T1D-induced testicular dysfunction and the potential mechanisms remain elusive. PURPOSE: The purpose of this present study was to investigate whether ICA ameliorates T1D-induced testicular dysfunction as well as its potential mechanisms. METHODS: T1D murine model was established by intraperitoneal injection of STZ with or without treated with ICA for eleven weeks. Morphological, pathological and serological experiments were used to determine the efficacy of ICA on male reproductive function of T1D mice. Western blotting, Immunohistochemistry analysis, qRT-PCR and kit determination were performed to investigated the underlying mechanisms. RESULTS: We found that replenishment of ICA alleviated testicular damage, promoted testosterone production and spermatogenesis, ameliorated apoptosis and blood testis barrier impairment in streptozotocin-induced T1D mice. Functionally, ICA treatment triggered adenosine monophosphate protein kinase (AMPK) activation, which in turn inhibited the nuclear translocation of nuclear factor kappa B p65 (NF-κB p65) to reduce inflammatory responses in the testis and activated nuclear factor erythroid 2-related factor 2(Nrf2), thereby enhancing testicular antioxidant capacity. Further studies revealed that supplementation with the AMPK antagonist Compound C or depletion of Nrf2 weakened the beneficial effects of ICA on testicular dysfunction of T1D mice. CONCLUSION: Collectively, these results demonstrate the feasibility of ICA in the treatment of T1D-induced testicular dysfunction, and reveal the important role of AMPK-mediated Nrf2 activation and NF-κB p65 inhibition in ICA-associated testicular protection during T1D.


Assuntos
Diabetes Mellitus Experimental , Diabetes Mellitus Tipo 1 , Flavonoides , Humanos , Criança , Camundongos , Masculino , Animais , Adolescente , NF-kappa B/metabolismo , Diabetes Mellitus Tipo 1/complicações , Diabetes Mellitus Tipo 1/tratamento farmacológico , Fator 2 Relacionado a NF-E2/metabolismo , Proteínas Quinases Ativadas por AMP , Diabetes Mellitus Experimental/complicações , Diabetes Mellitus Experimental/tratamento farmacológico
2.
Environ Sci Pollut Res Int ; 30(58): 121823-121833, 2023 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-37962761

RESUMO

Children aged 3-6 years undergo a critical stage of growth and development and are irreversibly affected by their iodine status. In order to reveal iodine status in preschool children, we detected iodine concentrations in urine samples from 1382 children aged 3-6 years based on a cross-sectional study. The median urinary iodine concentration (UIC) of children was 193.36 µg/L and was 336.96 µg/g·Cr corrected for creatinine. The study developed a link between dietary habits and iodine status, revealing that regular calcium supplement (OR: 1.79, (95% CI: 1.03, 3.12)) increased deficiency risk, while moderate seafood consumption (OR: 0.60, (95% CI: 0.38, 0.95)) decreased it. Additionally, modest intake of shellfish (OR: 0.58, (95% CI: 0.33, 1.00)), vegetables (OR: 0.61, (95% CI: 0.38, 0.97)), and eggs (OR: 0.53, (95% CI: 0.30, 0.95)) was found to protect against excess iodine. The findings underline the importance of balanced diets and various nutrients' roles in preschoolers' iodine status.


Assuntos
Iodo , Humanos , Pré-Escolar , Estudos Transversais , China , Nutrientes , Alimentos Marinhos , Estado Nutricional
3.
Plant Physiol ; 130(3): 1361-70, 2002 Nov.
Artigo em Inglês | MEDLINE | ID: mdl-12428001

RESUMO

Mineral nutrient deficiencies constitute major limitations for plant growth on agricultural soils around the world. To identify genes that possibly play roles in plant mineral nutrition, we recently generated a high-density array consisting of 1,280 genes from tomato (Lycopersicon esculentum) roots for expression profiling in nitrogen (N) nutrition. In the current study, we used the same array to search for genes induced by phosphorus (P), potassium (K(+)), and iron (Fe) deficiencies. RNA gel-blot analysis was conducted to study the time-dependent kinetics for expression of these genes in response to withholding P, K, or Fe. Genes previously not associated with P, K, and Fe nutrition were identified, such as transcription factor, mitogen-activated protein (MAP) kinase, MAP kinase kinase, and 14-3-3 proteins. Many of these genes were induced within 1 h after withholding the specific nutrient from roots of intact plants; thus, RNA gel-blot analysis was repeated for specific genes (transcription factor and MAP kinase) in roots of decapitated plants to investigate the tissue-specific location of the signal triggering gene induction. Both genes were induced just as rapidly in decapitated plants, suggesting that the rapid response to the absence of P, K, or Fe in the root-bathing medium is triggered either by a root-localized signal or because of root sensing of the mineral environment surrounding the roots. We also show that expression of Pi, K, and Fe transporter genes were up-regulated by all three treatments, suggesting coordination and coregulation of the uptake of these three essential mineral nutrients.


Assuntos
Ferro/farmacologia , Fósforo/farmacologia , Raízes de Plantas/genética , Potássio/farmacologia , Solanum lycopersicum/genética , Proteínas 14-3-3 , Regulação da Expressão Gênica de Plantas/efeitos dos fármacos , Transporte de Íons , Deficiências de Ferro , Solanum lycopersicum/metabolismo , Quinases de Proteína Quinase Ativadas por Mitógeno/genética , Quinases de Proteína Quinase Ativadas por Mitógeno/metabolismo , Proteínas Quinases Ativadas por Mitógeno/genética , Proteínas Quinases Ativadas por Mitógeno/metabolismo , Fósforo/deficiência , Raízes de Plantas/metabolismo , Potássio/metabolismo , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/genética , Fatores de Transcrição/genética , Fatores de Transcrição/metabolismo , Ativação Transcricional , Tirosina 3-Mono-Oxigenase/genética , Tirosina 3-Mono-Oxigenase/metabolismo
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