Antioxidant Biomarkers from Vanda coerulea Stems Reduce Irradiated HaCaT PGE-2 Production as a Result of COX-2 Inhibition

BACKGROUND: In our investigations towards the isolation of potentially biologically active constituents from Orchidaceae, we carried out phytochemical and biological analyses of Vanda species. A preliminary biological screening revealed that Vanda coerulea (Griff. ex. Lindl) crude hydro-alcoholic stem extract displayed the best DPPH /(•)OH radical scavenging activity and in vitro inhibition of type 2 prostaglandin (PGE-2) release from UV(B) (60 mJ/cm(2)) irradiated HaCaT keratinocytes. PRINCIPAL FINDINGS: Bio-guided fractionation and phytochemical analysis led to the isolation of five stilbenoids: imbricatin (1) methoxycoelonin (2) gigantol (3) flavidin (4) and coelonin (5). Stilbenoids (1-3) were the most concentrated in crude hydro-alcoholic stem extract and were considered as Vanda coerulea stem biomarkers. Dihydro-phenanthropyran (1) and dihydro-phenanthrene (2) displayed the best DPPH/(•)OH radical scavenging activities as well as HaCaT intracellular antioxidant properties (using DCFH-DA probe: IC(50) 8.8 µM and 9.4 µM, respectively) compared to bibenzyle (3) (IC(50) 20.6 µM). In turn, the latter showed a constant inhibition of PGE-2 production, stronger than stilbenoids (1) and (2) (IC(50) 12.2 µM and 19.3 µM, respectively). Western blot analysis revealed that stilbenoids (1-3) inhibited COX-2 expression at 23 µM. Interestingly, stilbenoids (1) and (2) but not (3) were able to inhibit human recombinant COX-2 activity. CONCLUSIONS: Major antioxidant stilbenoids (1-3) from Vanda coerulea stems displayed an inhibition of UV(B)-induced COX-2 expression. Imbricatin (1) and methoxycoelonin (2) were also able to inhibit COX-2 activity in a concentration-dependent manner thereby reducing PGE-2 production from irradiated HaCaT cells. Our studies suggest that stilbenoids (1-3) could be potentially used for skin protection against the damage caused by UV(B) exposure

Comparaison de différentes méthodes d'extraction d'acides dicaféoylquiniques à partir d'une plante halophile

AbstractThe aim of this study is the evaluation of different extraction methods for dicaffeoylquinic acids (diCQA), previously identified by a LC-DAD-ESI-QTOF dereplication strategy from a halophyte plant rich in polyphenols. Three different eco-friendly extraction methods are tested: microwave-assisted extraction (MAE), pressurized fluid extraction (PFE), supercritical fluid extraction (SFE). Various specific parameters are optimized for each of them. Global extraction yields are calculated for all extracts. Moreover, the extracts are analyzed by HPLC–DAD–ELSD, and the obtained profiles are compared to estimate qualitatively and semi-quantitatively their composition. The practicality of each technique is also discussed. The results show that the various parameters tested for PFE and MAE do not drastically affect the extraction of our interest compounds. However, the parameters tested on SFE are more decisive, such as the addition of a modifier in CO2, which allows the extraction of diCQA

Implicación de NF-κB y p53 en la expresión de receptores de muerte-TRAIL y apoptosis por procianidinas en células metastásicas humanas SW620

Introduction. The nuclear factor-kappaB (NF-κB) has been shown to upregulate pro-apoptotic mediators such as TRAIL-DR4/-DR5 receptors and the p53 transcription factor depending on the type of stimulus and the cell type involved. Previously, apple procyanidins (Pcy) have been shown to upregulate the expression of TRAIL-DR4/-DR5 and thereby overcoming the resistance of human colon cancer-derived metastatic SW620 cells to TRAIL.Objectives. NF-κB and p53 were investigated for their involvement in the Pcy-triggered apoptosis of human derived-metastatic colon cancer (SW620) cells.Materials and methods. Cell death, p53, TRAIL-DR4/-DR5 proteins were analyzed by flow cytometry. DR4/DR5 mRNA was analyzed by RT-PCR in real time. Activated p50/p65 and p53 forms were studied by ELISA and immunoblotting.Results. Pcy-triggered cell death was prevented by specific inhibitors of NF-κB and of p53: amino-4-(4-phenoxy-phenylethylamino) quinazoline (QNZ) and pifithrin α (Pα), respectively. QNZ and Pα inhibited the Pcy-dependent activation of TRAIL-DR4/-DR5 death receptors. However, the upregulation of TRAIL-DR4 by Pcy was significantly decreased only when NF-κB and p53 inhibitors were used in combination; this effect was not observed with a single inhibitor. This effect was not observed for TRAIL-DR5 and suggested that the expression of each TRAIL-death receptor may be regulated differently.Conclusions. These data suggested that NF-κB and p53 are partially required in Pcy-triggered apoptosis of SW620 cells by up-regulating the expression of TRAIL-DR4/-DR5. In addition, the ratio between TRAIL-DR4/-DR5 may be a determining factor in the activation of TRAIL-death receptor mediated apoptosis.  Introducción. Se ha demostrado que el factor nuclear-κB y p53 aumentan los mediadores proapoptósicos como los receptores de muerte TRAIL-DR4/-DR5, según el estímulo y el tipo celular. Previamente demostramos que las procianidinas de manzana aumentaban la expresión de TRAIL-DR4/-DR5, superando la resistencia a TRAIL característica en células humanas metastásicas SW620 derivadas del cáncer de colon.Objetivo. Investigar si NF-κB y p53 están involucrados en la apoptosis inducida por procianidinas en las células SW620.Materiales y métodos. La muerte celular y las proteínas p53, TRAIL-DR4/-DR5 se analizaron por citometría de flujo. Los ARN mensajeros (ARNm) de DR4/DR5 se analizaron por RT-PCR. Las formas activadas de p50/p65 y p53 se estudiaron por ELISA e inmunodetección.Resultados. La muerte celular activada por procianidinas fue prevenida por inhibidores específicos de NF-κB y de p53: amino-4-(4-fenoxi-feniletilamino)-quinazolina y pifitrina α, respectivamente. La quinazolina y la pifitrina α inhibieron la activación dependiente de procianidinas de TRAIL-DR4/DR5. Sin embargo, el aumento en la expresión de TRAIL-DR4 disminuyó significativamente sólo cuando la quinazolina y la pifitrina α se usaron simultáneamente; este efecto no se observó con cada uno por separado. No se observaron para TRAIL-DR5 estos efectos, lo cual sugiere que la expresión de cada receptor de muerte TRAIL puede estar regulada en forma diferente. Conclusiones. Estos datos sugieren que NF-κB y p53 se requieren parcialmente en la apoptosis de células SW620 inducida por procianidinas mediante el aumento en TRAIL-DR4/-DR5. La proporción de DR4/DR5 podría ser un factor determinante en la activación de la apoptosis por vía de TRAIL-DR4/-DR5

Activación diferencial de la apoptosis vía Fas (CD95) por procianidinas de manzana en células humanas de cáncer de colon y sus derivadas metastásicas

Introduction: We investigated the effects of apple procyanidins (Pcy), oligomers of catechins and epicatechins on Fas receptor expression and function in human colon adenocarcinoma cells (SW480) and in their derived metastatic cells (SW620). Methods: Pcy were characterized by reverse-phase HPLC. Cell death, Fas proteins, DNA fragmentation, and mitochondrial membrane potential were analyzed by flow cytometry. Fas mRNA was analyzed by RT-PCR in real time. Results: Pcy up-regulated the expression of the Fas receptor at the cell surface of both cell lines but activated Fas gene transcription only in SW620 cells. In SW480 cells, Pcy combined with Fas agonist CH-11 enhanced Fas-mediated apoptosis involving the loss of mitochondrial membrane potential and DNA fragmentation, which were abrogated by the antagonist antibody of Fas receptor, the anti-Fas ZB4. On the contrary, in SW620 cells, CH-11 was not able to enhance Pcy-triggered apoptosis indicating that Fas receptor-mediated apoptosis was not activated in these cells despite an up-regulation of Fas receptor gene expression. However, it was observed in SW620 cells that Pcy activated the Fas receptor-mediated apoptotic pathway after a specific blockage of TRAIL-death DR4/DR5 receptors. Conclusions: The present data showed that Pcy were able to activate the Fas receptor apoptotic pathway in SW480 cells and favored a cross-talk between TRAIL and Fas receptors in SW620 cells because specific blocking of TRAIL death receptors favored activation of the Fas receptor-mediated apoptosis. These important data may allow the emergence of new therapeutic protocols targeting death receptors against resistant metastatic cells. Introducción: Se estudiaron los efectos de procianidinas (Pcy) de manzana, oligómeros de catequinas y epicatequinas en la expresión y función del receptor Fas en células humanas de cáncer de colon (SW480) y sus derivadas metastásicas (SW620). Métodos: Las Pcy se caracterizaron por cromatografía líquida de alta presión (HPLC) en fase-reversa. Se analizaron por citometría de flujo la muerte celular, la proteína Fas, la fragmentación del ADN y el potencial de la membrana mitocondrial. Se analizaron los transcriptos de Fas por RT-PCR en tiempo real.Resultados: Las Pcy aumentaron la expresión del receptor Fas en la superficie celular de ambas líneas celulares pero la transcripción del gen Fas fue activado transcripcionalmente sólo en las células SW620. En las células SW480, las Pcy combinadas con el agonista de Fas CH-11 potenció la apoptosis mediada por Fas involucrando la pérdida del potencial mitocondrial de membrana y la fragmentación del ADN los cuales fueron evadidos por el anticuerpo antagonista del receptor Fas anti-ZB4. Por el contrario, en las células SW620, CH-11 no fue capaz de potenciar la apoptosis activada por Pcy indicando que la apoptosis mediada por el receptor Fas no fue activada en estas células a pesar del aumento en la expresión de Fas por regulación a nivel transcripcional. Sin embargo, se observó en las células SW620 que las Pcy activaron la vía apoptótica mediada por el receptor Fas después de un bloqueo específico de los receptores de muerte TRAIL DR4/DR5. Conclusiones: Estos datos muestran que las Pcy fueron capaces de activar la apoptosis a través del receptor Fas en las células SW480 y favorecieron una intercomunicación entre los receptores TRAIL y Fas en las células SW620 debido a que el bloqueo específico de los receptores de muerte TRAIL favoreció la activación de la apoptosis mediada por el receptor Fas. Estos datos podrían permitir el surgimiento de nuevos protocolos terapéuticos dirigidos contra receptores de muerte en células metastásicas resistentes

Methyl 5,7-dihydr­oxy-2,2,9-trimethyl-6,11-dioxo-6,11-dihydro-2H-anthra[2,3-b]pyran-8-carboxyl­ate

The title compound, C22H18O7, also known as laurentiquinone B, is a new anthraquinone which was isolated from Vismia laurentii, a Cameroonian medicinal plant. The asymmetric unit contains two independent mol­ecules. Each of them contains four fused rings, three of which are coplanar and typical of anthracene, while the heterocyclic rings adopt envelope conformations. Intra­molecular O—H⋯O hydrogen bonds result in the formation of two planar rings, which are also almost coplanar with the adjacent rings. In the crystal structure, inter­molecular O—H⋯O and C—H⋯O hydrogen bonds link the mol­ecules and a π–π contact is also present [centroid-centroid distance = 3.967 (3) Å]

Le pharmacien d'officine et la période périnatale (qualité du conseil et moyens d'action)

STRASBOURG ILLKIRCH-Pharmacie (672182101) / SudocSudocFranceF

Apports et limites des médecines alternatives et complémentaires dans la prise en charge de l'infertilité

STRASBOURG ILLKIRCH-Pharmacie (672182101) / SudocSudocFranceF

Les algues et leur potentiel cosmétique

STRASBOURG ILLKIRCH-Pharmacie (672182101) / SudocPARIS-BIUP (751062107) / SudocSudocFranceF

Bilan des connaissances scientifiques sur l'Arganier (Argania spinosa (L.) Skeels, Sapotaceae) (aspects botanique, chimique et pharmacologique)

STRASBOURG ILLKIRCH-Pharmacie (672182101) / SudocSudocFranceF

Propriétés pharmacologiques et risques toxicologiques de la muscade (myristica fragrans houtt.)

STRASBOURG ILLKIRCH-Pharmacie (672182101) / SudocSudocFranceF