Propolis is a complex phytocompound made from resinous and balsamic material harvested by bees from flowers, branches, pollen, and tree exudates.Humans have used propolis therapeutically for centuries. The aim of this article is to provide comprehensive review of the antiviral, antibacterial, antifungal, and antiparasitic properties of propolis. The mechanisms of action of propolis are discussed. There are two distinct impacts with regards to antimicrobial and anti-parasitic properties of propolis, on the pathogens and on the host. With regards to the pathogens, propolis acts by disrupting the ability of the pathogens to invade the host cells by forming a physical barrier and inhibiting enzymes and proteins needed for invasion into the host cells. Propolis also inhibits the replication process of the pathogens. Moreover, propolis inhibits the metabolic processes of the pathogens by disrupting cellular organelles and components responsible for energy production. With regard to the host, propolis functions as an immunomodulator. It upregulates the innate immunity and modulates the inflammatory signaling pathways. Propolis also helps maintain the host’s cellular antioxidant status. More importantly, a small number of human clinical trials have demonstrated the efficacy and the safety of propolis as an adjuvant therapy for pathogenic infections.

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Propolis is a resinous product collected by bees from plants to protect and maintain the homeostasis of their hives. Propolis has been used therapeutically by humans for centuries. This review article attempts to analyze the potential use of propolis in metabolic syndrome (MetS) and its associated chronic diseases. MetS and its chronic diseases were shown to be involved in at least seven out of the top 10 causes of death in 2019. Patients with MetS are also at a heightened risk of severe morbidity and mortality in the present COVID-19 pandemic. Propolis with its antioxidant and anti-inflammatory properties is potentially useful in ameliorating the symptoms of MetS and its associated chronic diseases. The aim of this article is to provide a comprehensive review on propolis and its therapeutic benefit in MetS and its chronic diseases, with an emphasis on in vitro and in vivo studies, as well as human clinical trials. Moreover, the molecular and biochemical mechanisms of action of propolis are also discussed. Propolis inhibits the development and manifestation of MetS and its chronic diseases by inhibiting of the expression and interaction of advanced glycation end products (AGEs) and their receptors (RAGEs), inhibiting pro-inflammatory signaling cascades, and promoting the cellular antioxidant systems.

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In recent years, research has demonstrated the efficacy propolis as a potential raw material for pharmaceuticals and nutraceuticals. There is limited report detailing the mechanisms of action of propolis and its bioactive compounds in relation to their anti-inflammatory properties. Thus, the aim of the present review is to examine the latest experimental evidence (2017–2022) regarding the anti-inflammatory properties of propolis. A systematic scoping review methodology was implemented. After applying the exclusion criteria, a total of 166 research publications were identified and retrieved from Scopus, Web of Science, and Pubmed. Several key themes related to the anti-inflammatory properties of propolis were subsequently identified, namely in relation to cancers, oral health, metabolic syndrome, organ toxicity and inflammation, immune system, wound healing, and pathogenic infections. Based on the latest experimental evidence, propolis is demonstrated to possess various mechanisms of action in modulating inflammation towards the regulatory balance and anti-inflammatory environment. In general, we summarize that propolis acts as an anti-inflammatory substance by inhibiting and downregulating TLR4, MyD88, IRAK4, TRIF, NLRP inflammasomes, NF-κB, and their associated pro-inflammatory cytokines such as IL-1β, IL-6, IFN-γ, and TNF-α. Propolis also reduces the migration of immune cells such as macrophages and neutrophils, possibly by downregulating the chemokines CXCL9 and CXCL10.