Effect of Silymarin and Harpagoside on Inflammation Reaction of BEAS-2B Cells, on Ciliary Beat Frequency (CBF) of Trachea Explants and on Mucociliary Clearance (MCC)
Institute of Pharmaceutical and Medicinal Chemistry-Pharmacology and Toxicology, University of Münster, Münster, Germany. Planta Medica
(Impact Factor: 2.15).
03/2012; 78(8):761-6. DOI: 10.1055/s-0031-1298374
Silymarin and harpagoside are derived from drugs which are used for their protective effects against hepatotoxicity and inflammatory processes. Both are now investigated with respect to the respiratory tract. They were able to reduce the release of the inflammatory cytokine RANTES (regulated on activation, normal T cells expressed and secreted) from BEAS-2B cells in a concentration-dependent manner when stimulated by a cytokine mix (10 ng/mL of TNF- α and IFN- γ). This effect was not due to a possible toxic effect (control experiments using LDH release as a marker). Silymarin but not harpagoside was able to increase ciliary beat frequency. Effects were comparable to positive controls (isoprenaline and salbutamol). Silymarin also increases mucociliary clearance. In conclusion, silymarin should be further investigated for its clinical use in distinct respiratory diseases.
Available from: onlinelibrary.wiley.com
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ABSTRACT: In this review, the evaluation methods for the screening of depigmenting substrates were investigated. For this purpose, the evaluation method of tyrosinase, a key enzyme of melanin biosynthesis, is most frequently used, but evaluating methods based on the regulation of cellular signal transfer factors or the inhibition of melanosome transfer have also been developed. Evaluation of the depigmenting effect using melanocytes is complex. It has the advantage of being capable of analysing overall effects on melanin biosynthesis at cellular levels. Before the final clinical testing of depigmenting agents, in vitro testing should be conducted to confirm the depigmenting efficacy and safety. Clinical studies for depigmenting agents can be used to investigate the prevention of melanin biosynthesis and to determine whether melanin disappears from skin. Therefore, the most appropriate protocol has to be employed, depending on the mechanism of action of the depigmenting agent.
Dans cette revue, les méthodes d'évaluation pour sélectionner des substances dépigmentantes ont été étudiées. Le procédé d'évaluation de la tyrosinase, enzyme clé de la biosynthèse de la mélanine, est le plus fréquemment utilisé, mais des méthodes de l'évaluation basées sur la régulation des facteurs de transfert de signaux cellulaires, ou sur l'inhibition du transfert des mélanosomes ont également été développées. L'évaluation de l'efficacité de dépigmentation à l'aide de mélanocytes est complexe. Elle a l'avantage d'être capable d'analyser l'ensemble des effets sur la biosynthèse de la mélanine au niveau cellulaire. Avant l'essai clinique final des agents de la dépigmentation, des tests in vitro doivent être menées pour confirmer l'efficacité dépigmentante et la sécurité. Les études cliniques d'agents dépigmentants peuvent être utilisées pour étudier la prévention de la biosynthèse de la mélanine et de déterminer si la mélanine de la peau disparaît. Par conséquent, le protocole le plus approprié doit être utilisé, en fonction du mécanisme d'action de l'agent dépigmentant.
International journal of cosmetic science 10/2012; 35(1). DOI:10.1111/ics.12012 · 1.38 Impact Factor
Available from: Milen I Georgiev
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ABSTRACT: Harpagoside is an iridoid glycoside that was first isolated from Harpagophytum
procumbens (devil’s claw, Pedaliaceae), a medicinal plant in which it is the major
constituent of the iridoid pool. Both the pure compound and devil’s claw extracts have
potent anti-rheumatic, anti-inflammatory and analgesic effects. According to the
European Pharmacopoeia commercial devil’s claw products should contain at least 1.2%
harpagoside. However, the compound has also been isolated from several other plant
species and in vitro plant culture systems. Recent advances in knowledge of harpagoside
distribution, biosynthesis/accumulation and pharmacology are summarized in this review.
We also discuss the possible synergism and/or antagonism between major constituents in
harpagoside-containing phytopharmaceutical products. Finally, future perspectives for its
potential application are highlighted.
Phytochemistry 04/2013; 92. DOI:10.1016/j.phytochem.2013.04.009 · 2.55 Impact Factor
Available from: Robson Seriani
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ABSTRACT: Particulate matter from diesel exhaust (DEP) has toxic properties and can activate intracellular signaling pathways and induce metabolic changes. This study was conducted to evaluate the activation of extracellular signal-regulated kinase (ERK) and c-Jun N-terminal kinase (JNK) and to analyze the mucin profile (acid (AB+), neutral (PAS+), or mixed (AB/PAS+) mucus) and vacuolization (V) of tracheal explants after treatment with 50 or 100 μg/mL DEP for 30 or 60 min. Western blot analyses showed small increases in ERK1/2 and JNK phosphorylation after 30 min of 100 μg/mL DEP treatment compared with the control. An increase in JNK phosphorylation was observed after 60 min of treatment with 50 μg/mL DEP compared with the control. We did not observe any change in the level of ERK1/2 phosphorylation after treatment with 50 μg/mL DEP. Other groups of tracheas were subjected to histological sectioning and stained with periodic acid-Schiff (PAS) reagent and Alcian Blue (AB). The stained tissue sections were then subjected to morphometric analysis. The results obtained were compared using ANOVA. Treatment with 50 μg/mL DEP for 30 min or 60 min showed a significant increase (p < 0.001) in the amount of acid mucus, a reduction in neutral mucus, a significant reduction in mixed mucus, and greater vacuolization. Our results suggest that compounds found in DEPs are able to activate acid mucus production and enhance vacuolization and cell signaling pathways, which can lead to airway diseases. © 2014 Wiley Periodicals, Inc. Environ Toxicol, 2014.
Environmental Toxicology 04/2014; 30(11). DOI:10.1002/tox.22000 · 3.20 Impact Factor
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