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1.
Int J Mol Sci ; 19(1)2018 Jan 18.
Artigo em Inglês | MEDLINE | ID: mdl-29346311

RESUMO

Cancer is a major cause of death. The outcomes of current therapeutic strategies against cancer often ironically lead to even increased mortality due to the subsequent drug resistance and to metastatic recurrence. Alternative medicines are thus urgently needed. Cumulative evidence has pointed out that pterostilbene (trans-3,5-dimethoxy-4-hydroxystilbene, PS) has excellent pharmacological benefits for the prevention and treatment for various types of cancer in their different stages of progression by evoking apoptotic or nonapoptotic anti-cancer activities. In this review article, we first update current knowledge regarding tumor progression toward accomplishment of metastasis. Subsequently, we review current literature regarding the anti-cancer activities of PS. Finally, we provide future perspectives to clinically utilize PS as novel cancer therapeutic remedies. We, therefore, conclude and propose that PS is one ideal alternative medicine to be administered in the diet as a nutritional supplement.


Assuntos
Antineoplásicos/farmacologia , Apoptose/efeitos dos fármacos , Estilbenos/farmacologia , Antineoplásicos/uso terapêutico , Terapias Complementares , Estresse do Retículo Endoplasmático/efeitos dos fármacos , Humanos , MicroRNAs/metabolismo , Metástase Neoplásica , Neoplasias/tratamento farmacológico , Neoplasias/patologia , Células Neoplásicas Circulantes/efeitos dos fármacos , Células Neoplásicas Circulantes/metabolismo , Estilbenos/uso terapêutico
2.
PLoS One ; 9(9): e108317, 2014.
Artigo em Inglês | MEDLINE | ID: mdl-25248126

RESUMO

Chromium hypersensitivity (chromium-induced allergic contact dermatitis) is an important issue in occupational skin disease. Hexavalent chromium (Cr (VI)) can activate the Akt, Nuclear factor κB (NF-κB), and Mitogen-activated protein kinase (MAPK) pathways and induce cell death, via the effects of reactive oxygen species (ROS). Recently, cell death stimuli have been proposed to regulate the release of inflammatory cytokines, such as tumor necrosis factor-α (TNF-α) and interleukin-1 (IL-1). However, the exact effects of ROS on the signaling molecules and cytotoxicity involved in Cr(VI)-induced hypersensitivity have not yet been fully demonstrated. N-acetylcysteine (NAC) could increase glutathione levels in the skin and act as an antioxidant. In this study, we investigated the effects of NAC on attenuating the Cr(VI)-triggered ROS signaling in both normal keratinocyte cells (HaCaT cells) and a guinea pig (GP) model. The results showed the induction of apoptosis, autophagy and ROS were observed after different concentrations of Cr(VI) treatment. HaCaT cells pretreated with NAC exhibited a decrease in apoptosis and autophagy, which could affect cell viability. In addition, Cr (VI) activated the Akt, NF-κB and MAPK pathways thereby increasing IL-1α and TNF-α production. However, all of these stimulation phenomena could be inhibited by NAC in both of in vitro and in vivo studies. These novel findings indicate that NAC may prevent the development of chromium hypersensitivity by inhibiting of ROS-induced cell death and cytokine expression.


Assuntos
Acetilcisteína/uso terapêutico , Antioxidantes/uso terapêutico , Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Cromo/toxicidade , Dermatite Alérgica de Contato/tratamento farmacológico , Interleucina-1alfa/biossíntese , Espécies Reativas de Oxigênio/antagonistas & inibidores , Transdução de Sinais/efeitos dos fármacos , Fator de Necrose Tumoral alfa/biossíntese , Acetilcisteína/farmacologia , Animais , Antioxidantes/farmacologia , Células Cultivadas , Dermatite Alérgica de Contato/etiologia , Dermatite Alérgica de Contato/patologia , Dermatite Alérgica de Contato/prevenção & controle , Avaliação Pré-Clínica de Medicamentos , Feminino , Regulação da Expressão Gênica/efeitos dos fármacos , Cobaias , Interleucina-1alfa/genética , Queratinócitos/efeitos dos fármacos , Queratinócitos/metabolismo , Sistema de Sinalização das MAP Quinases/efeitos dos fármacos , NF-kappa B/fisiologia , Proteína Oncogênica v-akt/fisiologia , RNA Mensageiro/biossíntese , RNA Mensageiro/genética , Fator de Necrose Tumoral alfa/genética
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