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.

Propolis is a resinous beehive product that is collected by the bees from plant resin and exudates, to protect and maintain hive homeostasis. Propolis has been used by humans therapeutically to treat many ailments including respiratory tract-related diseases and disorders. The aim of the present systematic scoping review is to evaluate the experimental evidence to support the use of propolis as a primary or an adjunctive therapy in respiratory tract-related diseases and disorders. After applying the exclusion criteria, 158 research publications were retrieved and identified from Scopus, Web of Science, Pubmed, and Google Scholar. The key themes of the included studies were pathogenic infection-related diseases and disorders, inflammation-related disorders, lung cancers, and adverse effects. Furthermore, the potential molecular and biochemical mechanisms of action of propolis in alleviating respiratory tract-related diseases and disorders are discussed. In conclusion, the therapeutic benefits of propolis have been demonstrated by various in vitro studies, in silico studies, animal models, and human clinical trials. Based on the weight and robustness of the available experimental and clinical evidence, propolis is effective, either as a primary or an adjunctive therapy, in treating respiratory tract-related diseases.

Autophagy is a degradation process that is evolutionarily conserved and is essential in maintaining cellular and physiological homeostasis through lysosomal removal and elimination of damaged peptides, proteins and cellular organelles. The dysregulation of autophagy is implicated in various diseases and disorders, including cancers, infection-related, and metabolic syndrome-related diseases. Propolis has been demonstrated in various studies including many human clinical trials to have antimicrobial, antioxidant, anti-inflammatory, immune-modulator, neuro-protective, and anti-cancer. Nevertheless, the autophagy modulation properties of propolis have not been extensively studied and explored. The role of propolis and its bioactive compounds in modulating cellular autophagy is possibly due to their dual role in redox balance and inflammation. The present review attempts to discuss the activities of propolis as an autophagy modulator in biological models in relation to various diseases/disorders which has implications in the development of propolis-based nutraceuticals, functional foods, and complementary therapies.

Obesity is a severe public health concern that can impair brain structure and function. The potential anti-inflammatory and anti-obesogenic properties of propolis extract are beneficial in preventing brain damage after diet-induced obesity. The purpose of the study is to investigate the role of propolis extract in high-fat diet-induced obesity rats using the Lee index and brain-body weight ratio (BBWR). We divided the rats into the experimental groups as follows: CD (normal chow diet), CP (normal chow diet with propolis treatment), FD (high-fat diet), and FP (high-fat diet with propolis treatment). We administered propolis extract in CP and FP for nine weeks during 21 weeks of diet. The rat's body weight and length were measured for obesity evaluation. The brain of all experimental rats was harvested and weighed at the end of the study. We found that a chronic high-fat diet significantly increased body weight and the Lee index (p < 0.01). However, a high-fat diet significantly decreased brain weight and BBWR in rats (p < 0.05). Nine weeks of propolis extract supplementation in the FP group reduced the Lee index (p < 0.01) and slightly increased brain weight and BBWR compared to the FD group. We observed a negative correlation between brain weight and the Lee index (R = – 0.64). Therefore, we conclude that propolis extract has the potential to sustain brain health in obesity.

Menopause is a natural part of the aging process that every woman experiences at some point in life. Menopausal symptoms have a negative impact on the quality of life. Common menopausal symptoms include vasomotor symptoms, mood swings, concentration issues, vaginal dryness, atrophy of secondary sexual traits, libido loss, musculoskeletal discomfort, osteopenia, and osteoporosis. The most effective treatment for the relief of menopausal symptoms is estrogen, with or without. Hormone replacement therapy (HRT) is most beneficial before 60 years of age or within 10 years of menopause. Other menopause-related symptoms including mood swings, sleep disturbance, sexual dysfunction, and myalgia may improve with HRT. HRT is also effective in preventing bone loss associated with menopause and in reducing the incidence of all osteoporosis-related fractures, including those of the vertebrae and hip.

Background: Dementia is a neurocognitive disorder associated with the aging brain and mainly affects the hippocampus and cerebral cortex. The Hippo signaling pathway and autophagy proteins have been found to be perturbed in the brain affected by dementia processes. Objective: This systematic review aims to elaborate on the involvement of the Hippo signaling pathway and autophagy in modulating the progression and severity of dementia in aging. Methods: Searches were conducted on MEDLINE, Google Scholar, Scopus, and Web of Science databases. Results: The Hippo signaling pathway is dependent upon the transcriptional co-activator YAP/TAZ, which forms complexes with TEAD in the nucleus in order to maintain cell homeostasis. When the expression YAP/TAZ is reduced, transcriptional repression-induced atypical cell death, ballooning cell death, and necrosis will consequently occur in the neurons. Moreover, the autophagic proteins, such as LC3, ATG proteins, and Beclin, are reduced, resulting in the disruption of autophagosome formation and accumulation and the spread of misfolded proteins in the brain suffering from dementia. Conclusion: The impairment of the Hippo signaling pathway and autophagy in the dementia process in aging should be considered since it might predict the severity, treatment, and prevention of dementia.