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Phytother Res ; 32(8): 1546-1554, 2018 Aug.
Artigo em Inglês | MEDLINE | ID: mdl-29672960


Thai herbal antipyretic 22 formula (APF22), a polyherbal formula, has been traditionally used to treat dermatologic problems including hyperpigmentation. Exposure of the skin to ultraviolet A (UVA) causes abnormal melanin production induced by photooxidative stress. This study thus aimed to investigate the protective effects of APF22 extracts and phenolic compounds, ferulic acid (FA), and gallic acid (GA; used as positive control and reference compounds), on melanogenesis through modulation of nuclear factor E2-related factor 2 (Nrf2) signaling and antioxidant defenses in mouse melanoma (B16F10) cells exposed to UVA. Our results revealed that the APF22 extracts, FA, and GA reduced melanin synthesis as well as activity and protein levels of tyrosinase in UVA-irradiated B16F10 cells. Moreover, APF22 extracts and both FA and GA were able to activate Nrf2-antioxidant response element signaling and promote antioxidant defenses including glutathione, catalase, glutathione peroxidase, and the glutathione-S-transferase at both mRNA and enzyme activity levels in irradiated cells. In conclusion, APF22 extracts suppressed UVA-mediated melanogenesis in B16F10 cells possibly via redox mechanisms involving activation of Nrf2 signaling and upregulation of antioxidant defenses. Moreover, pharmacological action of the APF22 extracts may be attributed to the phenolic compounds, FA, and GA, probably serving as the APF22's active compounds.

Antipiréticos/farmacologia , Melaninas/biossíntese , Extratos Vegetais/farmacologia , Raios Ultravioleta , Animais , Elementos de Resposta Antioxidante , Antioxidantes/metabolismo , Catalase/metabolismo , Linhagem Celular Tumoral , Ácidos Cumáricos/farmacologia , Ácido Gálico/farmacologia , Glutationa/metabolismo , Glutationa Peroxidase/metabolismo , Melanoma Experimental , Camundongos , Monofenol Mono-Oxigenase/antagonistas & inibidores , Fator 2 Relacionado a NF-E2/metabolismo , Oxirredução , Estresse Oxidativo/efeitos dos fármacos , Fenóis/farmacologia , Pele/efeitos dos fármacos , Tailândia
Redox Biol ; 8: 79-90, 2016 08.
Artigo em Inglês | MEDLINE | ID: mdl-26765101


Dietary phenolics may play a protective role in UV-mediated skin pigmentation through their antioxidant and UV-absorbing actions. In this study, we investigated whether genetic silencing of Nrf2, regulating the transcription of antioxidant genes, affected melanogenesis in primary human epidermal melanocytes (HEMn) and B16F10 melanoma cells subjected to UVA (8J/cm(2)) exposure. Then, we explored the antimelanogenic actions of phenolics; caffeic acid (CA) and ferulic acid (FA) providing partial UVA protection; quercetin (QU) and rutin (RU) providing strong UVA protection and; avobenzone (AV), an efficient UVA filter, in association with modulation of Nrf2-mediated antioxidant defenses in response to UVA insults in B16F10 cells. Upon oxidative insults, Nrf2 silencing promoted melanogenesis in both HEMn and B16F10 cells irradiated with UVA. Stimulation of melanogenesis by UVA correlated with increased ROS and oxidative DNA damage (8-OHdG), GSH depletion as well as a transient downregulation of Nrf2 nuclear translocation and of Nrf2-ARE signaling in B16F10 cells. All test compounds exerted antimelanogenic effects with respect to their abilities to reverse UVA-mediated oxidative damage as well as downregulation of Nrf2 activity and its target antioxidants (GCLC, GST and NQO1) in B16F10 cells. In conclusion, defective Nrf2 may promote melanogenesis under UVA irradiation through oxidative stress mechanisms. Compounds with antioxidant and/or UVA absorption properties could protect against UVA-induced melanogenesis through indirect regulatory effect on Nrf2-ARE pathway.

Antioxidantes/farmacologia , Suplementos Nutricionais , Melaninas/biossíntese , Fator 2 Relacionado a NF-E2/metabolismo , Fenóis/farmacologia , Substâncias Protetoras/farmacologia , Raios Ultravioleta , Animais , Elementos de Resposta Antioxidante , Vias Biossintéticas/efeitos dos fármacos , Vias Biossintéticas/efeitos da radiação , Dano ao DNA/efeitos dos fármacos , Desoxiguanosina/análogos & derivados , Desoxiguanosina/farmacologia , Técnicas de Silenciamento de Genes , Glutationa/metabolismo , Humanos , Melanócitos/efeitos dos fármacos , Melanócitos/metabolismo , Melanócitos/efeitos da radiação , Melanoma/genética , Melanoma/metabolismo , Melanoma Experimental , Camundongos , Monofenol Mono-Oxigenase/metabolismo , Fator 2 Relacionado a NF-E2/genética , Interferência de RNA , Espécies Reativas de Oxigênio/metabolismo , Transcrição Genética
Photochem Photobiol ; 88(4): 961-8, 2012.
Artigo em Inglês | MEDLINE | ID: mdl-22360712


Ultraviolet A (UVA) plays a vital role in the pathogenesis of premature skin aging through keratinocyte cytotoxicity and degradation of collagen, a main component of the extracellular matrix providing structural support. Oxidative stress caused by UVA irradiation can mediate induction of matrix metalloprotease-1 (MMP-1), a major enzyme responsible for collagen damage. Protection against UV-mediated disturbance of antioxidant defense system has been proposed as a possible mechanism by which botanical compounds slow down skin aging process. This study therefore aimed to assess inhibitory effects of caffeic acid (CA) and ferulic acid (FA), powerful plant-based phenolic antioxidants, on UVA-induced cytotoxicity and MMP-1 activity and mRNA level through modulation of antioxidant defense mechanism in immortalized human keratinocyte (HaCaT) cells. Pretreatment of the cells with CA or FA prior to UVA irradiation inhibited cytotoxicity, induction of MMP-1 activity and mRNA and oxidant formation. Moreover, CA and FA were able to up-regulate glutathione (GSH) content, γ-glutamate cysteine ligase (γ-GCL) mRNA as well as activities and mRNA expression of catalase and glutathione peroxidase (GPx) in irradiated cells. In conclusion, CA and FA provided protective effects on UVA-mediated MMP-1 induction in HaCaT cells possibly through restoration of antioxidant defense system at the cellular and molecular level.

Ácidos Cafeicos/farmacologia , Ácidos Cumáricos/farmacologia , Queratinócitos/efeitos dos fármacos , Metaloproteinase 1 da Matriz/metabolismo , Inibidores de Metaloproteinases de Matriz/farmacologia , Antioxidantes/metabolismo , Catalase/genética , Catalase/metabolismo , Linhagem Celular Transformada , Regulação da Expressão Gênica , Glutamato-Cisteína Ligase/genética , Glutamato-Cisteína Ligase/metabolismo , Glutationa/biossíntese , Glutationa Peroxidase/genética , Glutationa Peroxidase/metabolismo , Humanos , Queratinócitos/citologia , Queratinócitos/metabolismo , Queratinócitos/efeitos da radiação , Metaloproteinase 1 da Matriz/genética , Estresse Oxidativo/efeitos dos fármacos , Estresse Oxidativo/efeitos da radiação , RNA Mensageiro/biossíntese , Envelhecimento da Pele/efeitos dos fármacos , Envelhecimento da Pele/patologia , Envelhecimento da Pele/efeitos da radiação , Raios Ultravioleta
J Photochem Photobiol B ; 108: 16-22, 2012 Mar 01.
Artigo em Inglês | MEDLINE | ID: mdl-22244344


Oxidative stress has been suggested to play a role in ultraviolet A (UVA)-mediated melanogenesis. Glutathione (GSH) and GSH-related enzymes including γ-glutamate cysteine ligase (γ-GCL) and glutathione S-transferase (GST) are important antioxidant defenses responsible for maintaining cellular redox balance. Hence, improving GSH redox system to cope with oxidative insults may be essential for attenuation of abnormal melanin production. Gallic acid (GA), a dietary phenolic, has been shown to provide beneficial effects against hyperpigmentation possibly through its antioxidant properties. This study thus aimed to assess the antimelanogenic action of GA with regard to modulation of GSH-GCL system and GST in two melanoma cell lines, lightly pigmented G361 human melanoma and more pigmented B16F10 mouse melanoma cells, irradiated with UVA. G361 cells were shown to have lower basal GSH content and GST activity than B16F10 cells. Moreover, GA provided antimelanogenic effects in correlation with promotion of GSH levels, GST activity as well as γ-GCL and GST mRNA in both G361 and B16F10 cells at 2-h post-irradiation. In summary, GA exhibits protective effects on UVA-mediated melanogenesis possibly through improvement of GSH-related antioxidant defenses. Furthermore, different redox state in G361 and B16F10 cells may affect the responses of melanoma cells to GA.

Antioxidantes/farmacologia , Ácido Gálico/farmacologia , Glutationa/metabolismo , Melaninas/biossíntese , Raios Ultravioleta , Animais , Diferenciação Celular/efeitos dos fármacos , Linhagem Celular Tumoral , Glutamato-Cisteína Ligase/genética , Glutamato-Cisteína Ligase/metabolismo , Glutationa Transferase/genética , Glutationa Transferase/metabolismo , Humanos , Melaninas/metabolismo , Camundongos , Monofenol Mono-Oxigenase/genética , Monofenol Mono-Oxigenase/metabolismo , Oxirredução , Estresse Oxidativo/efeitos dos fármacos
Arch Pharm Res ; 34(5): 811-20, 2011 May.
Artigo em Inglês | MEDLINE | ID: mdl-21656367


Ascorbic acid (AA) has been well known as a skin whitening agent, although attempts have been made to evaluate its protective role against ultraviolet (UV)-induced skin hyperpigmentation or increased melanin production. While melanogenesis is a defense mechanism of the skin against UV irradiation, melanin overproduction may also contribute to melanoma initiation. UVA might play a role in melanogenesis through promoting oxidative stress, which occurs as the result of increased formation of oxidants and/or reactive nitrogen species (RNS) including nitric oxide (NO). Therefore, we investigated the antimelanogenic effect of AA (7.5-120 µM) in association with its inhibitory effect on UVA-induced oxidant formation, NO production through endothelial and inducible NO synthases (eNOS and iNOS) activation and impairment of antioxidant defense using G361 human melanoma cells. Our study demonstrated a comparable ability of AA with that of kojic acid, a well-known tyrosinase inhibitor in inhibiting mushroom tyrosinase. Melanin content was reduced by AA, but neither tyrosinase activity nor mRNA levels were reduced by AA at non-cytotoxic concentrations in UVA-irradiated G361 cells. AA was shown to inhibit UVA-mediated catalase (CAT) inactivation, glutathione (GSH) depletion, oxidant formation and NO production through suppression of eNOS and iNOS mRNA. We report herein that AA can protect against UVA-dependent melanogenesis possibly through the improvement of antioxidant defense capacity and inhibition of NO production through down-regulation of eNOS and iNOS mRNA.

Antioxidantes/farmacologia , Ácido Ascórbico/farmacologia , Melaninas/metabolismo , Melanócitos/efeitos dos fármacos , Óxido Nítrico/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Raios Ultravioleta , Catalase/metabolismo , Linhagem Celular Tumoral , Sobrevivência Celular/efeitos dos fármacos , Sobrevivência Celular/efeitos da radiação , Fármacos Dermatológicos/farmacologia , Inibidores Enzimáticos/metabolismo , Proteínas Fúngicas/antagonistas & inibidores , Proteínas Fúngicas/genética , Proteínas Fúngicas/metabolismo , Regulação Enzimológica da Expressão Gênica/efeitos dos fármacos , Regulação Enzimológica da Expressão Gênica/efeitos da radiação , Glutationa/metabolismo , Humanos , Melanócitos/metabolismo , Melanócitos/efeitos da radiação , Melanoma/prevenção & controle , Monofenol Mono-Oxigenase/antagonistas & inibidores , Monofenol Mono-Oxigenase/genética , Monofenol Mono-Oxigenase/metabolismo , Óxido Nítrico Sintase Tipo II/genética , Óxido Nítrico Sintase Tipo II/metabolismo , Óxido Nítrico Sintase Tipo III/genética , Óxido Nítrico Sintase Tipo III/metabolismo , RNA Mensageiro/metabolismo , Pigmentação da Pele/efeitos dos fármacos , Raios Ultravioleta/efeitos adversos
J Med Assoc Thai ; 93(1): 115-22, 2010 Jan.
Artigo em Inglês | MEDLINE | ID: mdl-20196420


INTRODUCTION: Ayurved Siriraj Chantaleela recipe is a traditional Thai remedy consisting of eight medicinal plants, which is employed for the treatment of fever. OBJECTIVE: To investigate the effects of Ayurved Siriraj Herbal recipe Chantaleela on platelet aggregation. STUDY DESIGN: Clinical research; ex vivo with before and after study design. MATERIAL AND METHOD: Twelve healthy male and female volunteers participated in the present study. Platelet aggregation test before Chantaleela ingestion was done as a control. After administration of 750 mg Chantaleela (3 x 250 mg tablets) every 8 hours for 3 doses, platelet aggregation was measured 8 hours following the first dose using an aggregometer and microplate reader. Adrenaline (Adr) and adenosine diphosphate (ADP) were used as platelet stimulants. Platelet aggregation was measured again at 32 hours and 8-10 days after the first dose. RESULTS: All of the participants completed the present study without any adverse event. Ayurved Siriraj Chantaleela did not affect platelet aggregation; neither Adr nor ADP were used as platelet agonists in both aggregometer and microplate reader Subgroup analysis revealed no significant change in platelet aggregation after Chantaleela administration according to the control for both male and female groups. The same results were also obtained in other subgroup analysis including hyperaggregation group, hypo-normal aggregation group. CONCLUSION: From the present study, normal dose of Chantaleela for alleviation of fever does not have an effect on either platelet aggregation or platelet numbers. It may conclude that the present study supports the safety use of Chantaleela for relieving fever as platelet status does not need to be taken into consideration.

Plaquetas/efeitos dos fármacos , Medicina Herbária , Medicina Ayurvédica , Agregação Plaquetária/efeitos dos fármacos , Administração Oral , Adulto , Análise de Variância , Avaliação de Medicamentos , Feminino , Humanos , Masculino , Tailândia