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1.
J Orthop Surg Res ; 18(1): 794, 2023 Oct 24.
Artigo em Inglês | MEDLINE | ID: mdl-37875949

RESUMO

BACKGROUND: Bone fragility is a recognized complication of type 1 diabetes (T1D). Thus, lower trabecular bone score (TBS) measurements in T1D patients can be predicted. However, the results of current studies on TBS in patients with T1D are inconsistent. In this context, the present study aimed to test the hypothesis that T1D is associated with lower TBS through a meta-analysis. METHODS: An electronic search of the literature was conducted using PubMed, Embase and Web of science databases to identify studies related to TBS and T1D, supplemented by an additional manual check of the reference list of relevant original and review articles. All data was analyzed using a random effects model. Results were compared using standardized mean differences (SMD) and 95% confidence intervals (CI). P ≤ 0.05 was considered statistically significant. Review Manager 5.4 software and Stata 17.0 software were used for statistical analysis. RESULTS: Seven cross-sectional studies involving 848 participants were included. TBS was lower in T1D patients than in healthy controls on random effects analysis, with no heterogeneity (SMD = - 0.39, 95% CI [- 0.53, - 0.24], P < 0.001; I2 = 0%). In addition, by subgroup analysis, T1D patients were strongly associated with reduced TBS in different regions and age groups, and the results were independent of covariate adjustment. CONCLUSION: This study showed that TBS was lower in patients with T1D than in healthy individuals with normal blood glucose levels, suggesting that TBS may be a useful measure to assess fracture risk in T1D.


Assuntos
Diabetes Mellitus Tipo 1 , Fraturas por Osteoporose , Humanos , Diabetes Mellitus Tipo 1/complicações , Densidade Óssea , Absorciometria de Fóton/métodos , Estudos Transversais , Osso Esponjoso/diagnóstico por imagem , Vértebras Lombares , Fraturas por Osteoporose/etiologia
2.
Hum Cell ; 31(3): 199-209, 2018 Jul.
Artigo em Inglês | MEDLINE | ID: mdl-29549584

RESUMO

Diabetic nephropathy (DN) is the major cause of end-stage renal disease in diabetic patients. Zicao, a well-known Chinese traditional medicine, has attracted much attention due to its beneficial effects in various medical fields. In this study, we attempted to investigate the effects and mechanisms of action of acetylshikonin, the main ingredient of Zicao, on renal dysfunction in DN. Our results showed that administration with acetylshikonin not only decreased blood urea nitrogen, urine creatinine and the mean kidney-to-body weight ratio in streptozotocin-induced diabetic mice, but also restored the loss of body weight, whereas the blood glucose was not changed. Masson's trichrome staining showed that acetylshikonin treatment resulted in a marked decrease in kidney fibrosis from diabetic mice. The increased expression of fibrosis proteins, such as plasminogen activator inhibitor type 1 (PAI-1), connective tissue growth factor, and collagen III and IV, were reduced after acetylshikonin administration. In addition, the expressions of interleukin-1ß, interleukin-6, monocyte chemoattractant protein-1, intercellular adhesion molecule 1 and infiltration of macrophages in kidney tissues were decreased in acetylshikonin-treated diabetic mice. Acetylshikonin led to a reduction of transforming growth factor-ß1 (TGF-ß1) expression and Smad-2/3 phosphorylation, as accompanied by increased Smad7 expression. Furthermore, in vitro treatment with acetylshikonin markedly attenuated TGF-ß1-induced the PAI-1, collagen III and IV, and Smad-2/3 phosphorylation in HK2 immortalized human proximal tubule epithelial cells. Acetylshikonin also prevented epithelial-to-mesenchymal transition induced by TGF-ß1. Collectively, our study provides evidences that acetylshikonin attenuates renal fibrosis though inhibiting TGF-ß1/Smad signaling pathway, suggesting that acetylshikonin may be a novel therapeutic agent for the treatment of DN.


Assuntos
Antraquinonas/farmacologia , Antraquinonas/uso terapêutico , Nefropatias Diabéticas/tratamento farmacológico , Nefropatias Diabéticas/patologia , Medicamentos de Ervas Chinesas/química , Rim/patologia , Fitoterapia , Proteínas Smad/metabolismo , Fator de Crescimento Transformador beta1/metabolismo , Animais , Antraquinonas/isolamento & purificação , Diabetes Mellitus Experimental , Nefropatias Diabéticas/genética , Nefropatias Diabéticas/metabolismo , Modelos Animais de Doenças , Transição Epitelial-Mesenquimal/efeitos dos fármacos , Fibrose , Expressão Gênica/efeitos dos fármacos , Masculino , Camundongos Endogâmicos C57BL , Fosforilação/efeitos dos fármacos , Transdução de Sinais/efeitos dos fármacos , Transdução de Sinais/genética , Estreptozocina , Fator de Crescimento Transformador beta1/genética
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