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Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents

Background: Phosphodiesterases (PDEs) play a major role in the regulation of cyclic adenosine monophosphate (cAMP)- and cyclic guanosine monophosphate (cGMP)-mediated pathways. Their inhibitors exhibit anti-inflammatory, vasodilatory and antithrombotic effects. Therefore, consumption of foods with P...

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Autores principales: Röhrig, Teresa, Pacjuk, Olga, Hernández-Huguet, Silvia, Körner, Johanna, Scherer, Katharina, Richling, Elke
Formato: Online Artículo Texto
Lenguaje:English
Publicado: MDPI 2017
Materias:
Acceso en línea:https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5750604/
https://www.ncbi.nlm.nih.gov/pubmed/29113064
http://dx.doi.org/10.3390/medicines4040080
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author Röhrig, Teresa
Pacjuk, Olga
Hernández-Huguet, Silvia
Körner, Johanna
Scherer, Katharina
Richling, Elke
author_facet Röhrig, Teresa
Pacjuk, Olga
Hernández-Huguet, Silvia
Körner, Johanna
Scherer, Katharina
Richling, Elke
author_sort Röhrig, Teresa
collection PubMed
description Background: Phosphodiesterases (PDEs) play a major role in the regulation of cyclic adenosine monophosphate (cAMP)- and cyclic guanosine monophosphate (cGMP)-mediated pathways. Their inhibitors exhibit anti-inflammatory, vasodilatory and antithrombotic effects. Therefore, consumption of foods with PDE-inhibiting potential may possess beneficial influence on the risk of cardiovascular diseases. Methods: Four plant extracts (Arbutus unedo, Camellia sinensis, Cynara scolymus, Zingiber officinale) with promising ingredient profiles and physiological effects were tested for their ability to inhibit cAMP-specific PDE in vitro in a radioactive assay. Results: Strawberry tree fruit (Arbutus unedo) and tea (Camellia sinensis) extracts did not inhibit PDE markedly. Alternatively, artichoke (Cynara scolymus) extract had a significant inhibitory influence on PDE activity (IC(50) = 0.9 ± 0.1 mg/mL) as well as its flavone luteolin (IC(50) = 41 ± 10 μM) and 3,4-dicaffeoylquinic acid (IC(50) > 1.0 mM). Additionally, the ginger (Zingiber officinale) extract and one of its constituents, [6]-gingerol, significantly inhibited PDE (IC(50) = 1.7 ± 0.2 mg/mL and IC(50) > 1.7 mM, respectively). Crude fractionation of ginger extract showed that substances responsible for PDE inhibition were in the lipoid fraction (IC(50) = 455 ± 19 μg/mL). Conclusions: A PDE-inhibitory effect was shown for artichoke and ginger extract. Whether PDE inhibition in vivo can be achieved through ingestion of artichoke or ginger extracts leading to physiological effects concerning cardiovascular health should be addressed in future research.
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spelling pubmed-57506042018-01-08 Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents Röhrig, Teresa Pacjuk, Olga Hernández-Huguet, Silvia Körner, Johanna Scherer, Katharina Richling, Elke Medicines (Basel) Article Background: Phosphodiesterases (PDEs) play a major role in the regulation of cyclic adenosine monophosphate (cAMP)- and cyclic guanosine monophosphate (cGMP)-mediated pathways. Their inhibitors exhibit anti-inflammatory, vasodilatory and antithrombotic effects. Therefore, consumption of foods with PDE-inhibiting potential may possess beneficial influence on the risk of cardiovascular diseases. Methods: Four plant extracts (Arbutus unedo, Camellia sinensis, Cynara scolymus, Zingiber officinale) with promising ingredient profiles and physiological effects were tested for their ability to inhibit cAMP-specific PDE in vitro in a radioactive assay. Results: Strawberry tree fruit (Arbutus unedo) and tea (Camellia sinensis) extracts did not inhibit PDE markedly. Alternatively, artichoke (Cynara scolymus) extract had a significant inhibitory influence on PDE activity (IC(50) = 0.9 ± 0.1 mg/mL) as well as its flavone luteolin (IC(50) = 41 ± 10 μM) and 3,4-dicaffeoylquinic acid (IC(50) > 1.0 mM). Additionally, the ginger (Zingiber officinale) extract and one of its constituents, [6]-gingerol, significantly inhibited PDE (IC(50) = 1.7 ± 0.2 mg/mL and IC(50) > 1.7 mM, respectively). Crude fractionation of ginger extract showed that substances responsible for PDE inhibition were in the lipoid fraction (IC(50) = 455 ± 19 μg/mL). Conclusions: A PDE-inhibitory effect was shown for artichoke and ginger extract. Whether PDE inhibition in vivo can be achieved through ingestion of artichoke or ginger extracts leading to physiological effects concerning cardiovascular health should be addressed in future research. MDPI 2017-11-04 /pmc/articles/PMC5750604/ /pubmed/29113064 http://dx.doi.org/10.3390/medicines4040080 Text en © 2017 by the authors. Licensee MDPI, Basel, Switzerland. This article is an open access article distributed under the terms and conditions of the Creative Commons Attribution (CC BY) license (http://creativecommons.org/licenses/by/4.0/).
spellingShingle Article
Röhrig, Teresa
Pacjuk, Olga
Hernández-Huguet, Silvia
Körner, Johanna
Scherer, Katharina
Richling, Elke
Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents
title Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents
title_full Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents
title_fullStr Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents
title_full_unstemmed Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents
title_short Inhibition of Cyclic Adenosine Monophosphate-Specific Phosphodiesterase by Various Food Plant-Derived Phytotherapeutic Agents
title_sort inhibition of cyclic adenosine monophosphate-specific phosphodiesterase by various food plant-derived phytotherapeutic agents
topic Article
url https://www.ncbi.nlm.nih.gov/pmc/articles/PMC5750604/
https://www.ncbi.nlm.nih.gov/pubmed/29113064
http://dx.doi.org/10.3390/medicines4040080
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