Search

Propolis is produced by honey bees from a series of resinous, gummy and balsamic substances collected from the leaf buds of different tree species and mixed with their secretions. It is used as a sealant and antiseptic in the hive. Because of its antimicrobial properties, propolis has become a popular alternative medicine or food for health protection and disease prevention. The presence of a large number of flavonoids, aromatic acids and phenolic compounds has been suggested to be responsible for most biological and pharmacological activities of propolis. This review aims to provide a critical analysis of the different studies which evaluate the activity of propolis against fungi and to identify the chemical components responsible for such activity. The discussion of the methodological approaches used and the issued results is a key point of this review to highlight knowledge gaps. This review will first describe the chemical composition of the propolis and the factors of variability including geographical and botanical origins and then examine its antifungal activities with a focus against phytopathogenic fungi. Finally, it will discuss the main components responsible for such activities and their mechanism of action.

Propolis, a natural resinous mixture rich in polyphenols, produced by bees from a variety of plant sources, has shown significant therapeutic effects and may prevent the development of certain chronic diseases like type 2 diabetes mellitus (T2DM). The objective of this study was to evaluate the effect of supplementation with standardized poplar propolis extract powder (PPEP) on insulin homeostasis in non-diabetic insulin-resistant volunteers with obesity. In this randomized, controlled, crossover trial, nine non-diabetic insulin-resistant volunteers with obesity, aged 49 ± 7 years, were subjected to two periods of supplementation (placebo and PPEP) for 3 months. Blood samples and anthropomorphic data were collected at baseline and at the end of each phase of the intervention. PPEP supplementation improved insulin sensitivity by significantly decreasing the percentage of insulin-resistant subjects and the insulin sensitivity Matsuda index (ISI-M). According to this study, supplementation with standardized PPEP for 3 months in non-diabetic insulin-resistant volunteers with obesity led to an improvement in insulin homeostasis by its effect on insulin resistance and secretion. This study suggests that poplar propolis has a preventive effect on the physiopathological mechanisms of T2DM and, therefore, that it can help to prevent the development of the disease. [ABSTRACT FROM AUTHOR]

[beta],[beta]-Carotene 15,15'-monooxygenase (formerly termed [beta],[beta]-carotene 15,15'-dioxygenase, EC 1.13.11.21) catalyzes the conversion of provitamin A carotenoids to retinal in vertebrate tissues. In the present study, we investigated whether preformed vitamin A or [beta]-carotene and its direct metabolites can regulate the enzyme activity in vivo. We found dose-dependent decreases in intestinal [beta],[beta]-carotene monooxygenase activity after oral administration to rats of retinyl acetate (up to -79%), [beta]-carotene (up to -79%), apo-8'-carotenal (up to -56%), all-trans retinoic acid (up to -88%), and 9-cis retinoic acid (up to -67%). Liver [beta],[beta]-carotene 15,15'-monooxygenase ([beta]CMOOX) activity was not affected. Apo-12'carotenal and the retinoic acid receptor (RAR) [alpha] antagonist Ro 41-5253 significantly increased the intestinal enzyme activity by 55 and 94%, respectively. When [beta]-carotene was administered to rats pretreated with the two cytochrome [P.sub.450] (CYP) inducers, pentobarbital and naphthoflavone, the intestinal [beta]CMOOX activity increased by 39%. In a transcriptional study in chickens, treatment with retinoic acid resulted in low expression of the intestinal [beta]CMOOX. Our data suggest that retinoids and carotenoids might regulate [beta]CMOOX expression by a transcriptional feedback mechanism via interaction with members of the RAR family. J. Nutr. 132: 3616-3622, 2002. KEY WORDS: * [beta]-carotene cleavage * retinoic acid regulation * RAR[alpha] * rats * chickens

Background: The primary role of polymorphonuclear neutrophils (PMNs) is to destroy pathogenic microorganisms after phagocytosis by producing reactive oxygen species (ROS) and toxic molecules. However, PMNs produce sufficient amounts of ROS during an oxidative burst to be autotoxic and detrimental to their own functions and to possibly cause DNA damage, protein and lipid oxidation and cell membrane destructuration., Objective: The aim of this study was to investigate in vivo the role of the antioxidant capacities of carotenoids in modulating ROS content in PMNs during oxidative burst. Moreover to investigate the direct or indirect effect of carotenoids, the modification of PMN ROS content was explored after in vitro supplementation with beta-carotene or lycopene, chosen taking account of their vitamin A and no vitamin A precursor effect, respectively., Design: In vivo study: Venous blood was collected from 10 healthy male volunteers and ROS production from phorbol myristate acetate (PMA)-stimulated PMNs was determined, by flow cytometry using the fluorescent dye dihydrorhodamine 123, at baseline, after 3 weeks of carotenoid depletion (carotenoid intake limited to 25% of usual intake) and after 5 weeks of carotenoid repletion (30 mg beta-carotene, 15 mg lycopene and 9 mg lutein per day). In vitro study: ROS content in PMA-stimulated PMNs isolated from carotenoid depleted subjects and controls was quantified after an in vitro enrichment with beta-carotene (1 micromol/L) or lycopene (0.3 micromol/L)., Results: In vivo carotenoid depletion increased PMN H2O2 content after PMA activation by 38% (p < 0.05 vs baseline),while supplementation for 5 weeks restored basal H2O2 generation (p < 0.05 vs depletion). Although H2O2 measurement in PMNs from non-depleted subjects was not affected by an in vitro supply with beta-carotene or lycopene, a significant decrease in H2O2 content by 78.9 % and 81.2%, respectively, was observed in PMNs from carotenoid depleted subjects (p < 0.01 vs depleted control subjects)., Conclusions: The carotenoid ROS quenching capacities control both in vivo and in vitro the PMNs ROS generation and probably protect these cells against DNA, membrane lipid and protein damages during oxidative burst. Moreover, these effects appear independent from the metabolic conversion of carotenoids to vitamin A.