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1.
J. appl. oral sci ; 26: e20170004, 2018. tab, graf
Artículo en Inglés | LILACS, BBO | ID: biblio-893706

RESUMEN

ABSTRACT Among the many graft materials that have been used for the treatment of bone defects in oral and maxillofacial regions is xenograft. To improve osteoconductive effects of xenografts, they have been combined with various biocompatible materials, such as hyaluronic acid and bone morphogenetic protein. Objective: To determine bone-healing capacity of high molecular weight hyaluronic acid (HA) combined with xenograft in rabbit calvarial bone defects. Material and methods: Ten adult male New Zealand rabbits (mean weight 3 kg) were included in the study. Three 6-mm-diameter bicortical cranial defects were created on calvarial bone of all rabbits. These defects were filled as follows: a) xenograft; b) HA+xenograft; c) autograft. One month after the first operation, rabbits were sacrificed. Specimens were evaluated histomorphometrically. Results: Considering multiple comparisons, differences regarding new bone were statistically significant between all groups (p<0.05). The volume of residual graft was significantly decreased in HA group compared to xenograft group (p=0.035). Marrow space, trabecular thickness (TbTh), trabecular width (TbWi), trabecular separation (TbSp), and number of node: number of terminus (NNd:NTm) in the autograft group were significantly better than xenograft and HA groups (p<0.05). However, regarding marrow space, TbTh, TbWi, TbSp, and NNd:NTm values, xenograft and HA groups showed similar results and the difference were not significant (p>0.05). Conclusion: These results support that high molecular weight hyaluronic acid could contribute to the healing of xenograft by improving the percentage of new bone formation and reducing the percentage of residual graft. However, HA did not significantly affect the quality of newly formed bone assessed by microarchitectural parameters.


Asunto(s)
Humanos , Animales , Masculino , Cráneo/trasplante , Cicatrización de Heridas/efectos de los fármacos , Regeneración Ósea/efectos de los fármacos , Xenoinjertos/efectos de los fármacos , Ácido Hialurónico/farmacología , Conejos , Cráneo/efectos de los fármacos , Materiales Biocompatibles/farmacología , Reproducibilidad de los Resultados , Trasplante Óseo/métodos , Resultado del Tratamiento , Modelos Animales de Enfermedad , Autoinjertos/efectos de los fármacos , Hueso Esponjoso/efectos de los fármacos , Ácido Hialurónico/química , Peso Molecular
2.
Braz. j. med. biol. res ; 47(12): 1021-1028, 12/2014. tab, graf
Artículo en Inglés | LILACS | ID: lil-727663

RESUMEN

DNA hypomethylation may activate oncogene transcription, thus promoting carcinogenesis and tumor development. S-adenosylmethionine (SAM) is a methyl donor in numerous methylation reactions and acts as an inhibitor of intracellular demethylase activity, which results in hypermethylation of DNA. The main objectives of this study were to determine whether DNA hypomethylation correlated with vascular endothelial growth factor-C (VEGF-C) expression, and the effect of SAM on VEGF-C methylation and gastric cancer growth inhibition. VEGF-C expression was assayed by Western blotting and RT-qPCR in gastric cancer cells, and by immunohistochemistry in tumor xenografts. VEGF-C methylation was assayed by bisulfite DNA sequencing. The effect of SAM on cell apoptosis was assayed by flow cytometry analyses and its effect on cancer growth was assessed in nude mice. The VEGF-C promoters of MGC-803, BGC-823, and SGC-7901 gastric cancer cells, which normally express VEGF-C, were nearly unmethylated. After SAM treatment, the VEGF-C promoters in these cells were highly methylated and VEGF-C expression was downregulated. SAM also significantly inhibited tumor growth in vitro and in vivo. DNA methylation regulates expression of VEGF-C. SAM can effectively induce VEGF-C methylation, reduce the expression of VEGF-C, and inhibit tumor growth. SAM has potential as a drug therapy to silence oncogenes and block the progression of gastric cancer.


Asunto(s)
Animales , Humanos , Masculino , Antineoplásicos/farmacología , Metilación de ADN/efectos de los fármacos , Regulación hacia Abajo/efectos de los fármacos , Regulación Neoplásica de la Expresión Génica/efectos de los fármacos , S-Adenosilmetionina/farmacología , Neoplasias Gástricas/tratamiento farmacológico , Factor C de Crecimiento Endotelial Vascular/metabolismo , Apoptosis/efectos de los fármacos , Western Blotting , Línea Celular Tumoral , Carcinogénesis/efectos de los fármacos , Metilación de ADN/genética , Citometría de Flujo , Regulación Neoplásica de la Expresión Génica/fisiología , Xenoinjertos/efectos de los fármacos , Inmunohistoquímica , Ratones Desnudos , Oncogenes/efectos de los fármacos , Regiones Promotoras Genéticas/efectos de los fármacos , Reacción en Cadena en Tiempo Real de la Polimerasa , ARN Mensajero/análisis , Neoplasias Gástricas/metabolismo , Factor C de Crecimiento Endotelial Vascular/efectos de los fármacos , Factor C de Crecimiento Endotelial Vascular/genética
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