Your browser doesn't support javascript.
loading
Mostrar: 20 | 50 | 100
Resultados 1 - 2 de 2
Filtrar
Mais filtros











Base de dados
Intervalo de ano de publicação
1.
Wounds ; 27(12): 336-46, 2015 Dec.
Artigo em Inglês | MEDLINE | ID: mdl-27447106

RESUMO

UNLABELLED: New treatments are needed as infection risk associated with diabetic, venous, and pressure ulcers are becoming more prevalent as comorbidities of obesity, aging, and major disease. Postsurgical, burn, and immunocompromised patients are also at an increased risk of wounds and infection. Silver has been utilized in treating various wounds associated with infections and, although highly effective, caution is required for use beyond 2 weeks due to potential silver cytotoxicity. To overcome this obstacle, an antimicrobial wound gel (CelaCare Technologies, Inc, Dallas, TX) was designed to allow low concentrations of a proprietary silver salt combined with acemannan, which has been demonstrated to aid wound healing. MATERIALS AND METHODS: This study's objective was to determine the time-kill kinetics of the antimicrobial wound gel vs 4 commercial topical silver products against 6 common wound pathogens and Bacillus subtilis as a spore-forming bacteria. RESULTS: The antimicrobial wound gel achieved a 2.9 log reduction in growth of Pseudomonas aeruginosa within 30 minutes, a 2.3 log reduction in Streptococcus pyogenes within 8 hours, a 2.1 log reduction in methicillin-resistant Staphylococcus aureus within 48 hours, a 2.3 log reduction in S. aureus within 24 hours, a 4.1 log reduction in Escherichia coli within 30 minutes, a 2.9 log reduction in B. subtilis within 60 minutes, and a 3.4 log reduction in Candida albicans within 90 minutes. Overall, the antimicrobial wound gel demonstrated broad antimicrobial coverage against all wound pathogens evaluated, and it was comparable to, or better than, other tested topical silver products containing substantially higher silver concentrations. CONCLUSION: The broad-spectrum antimicrobial activity of the wound gel indicates it could become a product alternative to current commercial products.


Assuntos
Anti-Infecciosos/administração & dosagem , Anti-Infecciosos/farmacologia , Compostos de Prata/administração & dosagem , Compostos de Prata/farmacologia , Infecção dos Ferimentos/microbiologia , Administração Tópica , Bandagens , Candida albicans/efeitos dos fármacos , Escherichia coli/efeitos dos fármacos , Géis/administração & dosagem , Géis/farmacologia , Humanos , Staphylococcus aureus Resistente à Meticilina/efeitos dos fármacos , Testes de Sensibilidade Microbiana , Pseudomonas aeruginosa/efeitos dos fármacos , Úlcera Cutânea/microbiologia , Staphylococcus aureus/efeitos dos fármacos , Fatores de Tempo , Resultado do Tratamento , Cicatrização/efeitos dos fármacos
2.
Biochem Pharmacol ; 89(4): 515-25, 2014 Jun 15.
Artigo em Inglês | MEDLINE | ID: mdl-24735611

RESUMO

The ligation of interleukin-1 receptor (IL-1R) or tumor necrosis factor receptor 1 (TNFR1) induces the recruitment of adaptor proteins and their concomitant ubiquitination to the proximal receptor signaling complex, respectively. Such are upstream signaling events of IKK that play essential roles in NF-κB activation. Thus, the discovery of a substance that would modulate the recruitment of key proximal signaling elements at the upstream level of IKK has been impending in this field of study. Here, we propose that brazilin, an active compound of Caesalpinia sappan L. (Leguminosae), is a potent NF-κB inhibitor that selectively disrupts the formation of the upstream IL-1R signaling complex. Analysis of upstream signaling events revealed that brazilin markedly abolished the IL-1ß-induced polyubiquitination of IRAK1 and its interaction with IKK-γ counterpart. Notably, pretreatment of brazilin drastically interfered the recruitment of the receptor-proximal signaling components including IRAK1/4 and TRAF6 onto MyD88 in IL-1R-triggerd NF-κB activation. Interestingly, brazilin did not affect the TNF-induced RIP1 ubiquitination and the recruitment of RIP1 and TRAF2 to TNFR1, suggesting that brazilin is effective in selectively suppressing the proximal signaling complex formation of IL-1R, but not that of TNFR1. Moreover, our findings suggest that such a disruption of IL-1R-proximal complex formation by brazilin is not mediated by affecting the heterodimerization of IL-1R and IL-1RAcP. Taken together, the results suggest that the anti-IKK activity of brazilin is induced by targeting IKK upstream signaling components and subsequently disrupting proximal IL-1 receptor signaling complex formation.


Assuntos
Anti-Inflamatórios não Esteroides/farmacologia , Benzopiranos/farmacologia , Quinase I-kappa B/antagonistas & inibidores , Quinases Associadas a Receptores de Interleucina-1/antagonistas & inibidores , Transdução de Sinais/efeitos dos fármacos , Receptor 4 Toll-Like/antagonistas & inibidores , Anti-Inflamatórios não Esteroides/química , Anti-Inflamatórios não Esteroides/isolamento & purificação , Benzopiranos/química , Benzopiranos/isolamento & purificação , Caesalpinia/química , Etnofarmacologia , Genes Reporter/efeitos dos fármacos , Células HEK293 , Células HeLa , Humanos , Quinase I-kappa B/metabolismo , Proteínas I-kappa B/antagonistas & inibidores , Proteínas I-kappa B/genética , Proteínas I-kappa B/metabolismo , Quinases Associadas a Receptores de Interleucina-1/genética , Quinases Associadas a Receptores de Interleucina-1/metabolismo , Interleucina-1beta/antagonistas & inibidores , Interleucina-1beta/genética , Interleucina-1beta/metabolismo , Estrutura Molecular , NF-kappa B/agonistas , NF-kappa B/antagonistas & inibidores , NF-kappa B/genética , NF-kappa B/metabolismo , Receptores de Interleucina-1/agonistas , Receptores de Interleucina-1/antagonistas & inibidores , Receptores de Interleucina-1/genética , Receptores de Interleucina-1/metabolismo , Proteínas Recombinantes/química , Proteínas Recombinantes/metabolismo , República da Coreia , Receptor 4 Toll-Like/genética , Receptor 4 Toll-Like/metabolismo , Fator de Necrose Tumoral alfa/antagonistas & inibidores , Fator de Necrose Tumoral alfa/genética , Fator de Necrose Tumoral alfa/metabolismo , Ubiquitinação/efeitos dos fármacos , Madeira/química
SELEÇÃO DE REFERÊNCIAS
DETALHE DA PESQUISA