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High-fat diet (HFD) lifestyle contributes to global morbidity and mortality due to obesity. As a potential therapy candidate, propolis modulates gut microbiota affected by HFD through direct and indirect stimulation. This study investigates the effect of propolis on gut microbiota and ileum mucosal structure, using histological analyses to validate its efficacy in HFD intervention. Male Wistar rats were randomly assigned to one of four diet groups. Fecal microbiota analysis focusing on B. thetaiotaomicron, F. prausnitzii was conducted over several weeks using 16S rDNA sequencing. In addition, ileum mucosal changes were analyzed post-termination. The novelty of propolis intervention was observed in counteracting the burden of B. thetaiotaomicron, an inflammation indicator, through indirect stimulation, which led to an increase in F. prausnitzii. Propolis affected bacterial diversity through direct and indirect stimulation, resulting in B. thetaiotaomicron and F. prausnitzii reduced and achieved homeostasis at the end of the intervention. The overall bacterial profile showed a significantly higher relative ratio of F. prausnitzii to B. thetaiotaomicron between HFDP to NCD, NCDP (p<0.05). Validation through ileum histology revealed that the HFD group had reduced muscle thickness, fewer Peyer's patches, and fewer villi than the NCD group (p<0.05). The HFDP group showed significantly more villi and Peyer's patches than the HFD group (p<0.05). Propolis effectively ameliorated the dysbiotic state of the gut microbiome, helping achieve favorable homeostasis. The HFDP group showed no significant differences compared to the NCD group, indicating the protective effect of propolis on the structure and physiological functions of the gastrointestinal system. [ABSTRACT FROM AUTHOR]

Stroke is the world's second-leading cause of death. Current treatments for cerebral edema following intracerebral hemorrhage (ICH) mainly involve hyperosmolar fluids, but this approach is often inadequate. Propolis, known for its various beneficial properties, especially antioxidant and anti-inflammatory properties, could potentially act as an adjunctive therapy and help alleviate stroke-associated injuries. The chemical composition of Geniotrigona thoracica propolis extract was analyzed by GC-MS after derivatization for its total phenolic and total flavonoid content. The total phenolic content and total flavonoid content of the propolis extract were 1037.31 ± 24.10 μg GAE/mL and 374.02 ± 3.36 μg QE/mL, respectively. By GC-MS analysis, its major constituents were found to be triterpenoids (22.4% of TIC). Minor compounds, such as phenolic lipids (6.7% of TIC, GC-MS) and diterpenic acids (2.3% of TIC, GC-MS), were also found. Ninety-six Sprague Dawley rats were divided into six groups; namely, the control group, the ICH group, and four ICH groups that received the following therapies: mannitol, propolis extract (daily oral propolis administration after the ICH induction), propolis-M (propolis and mannitol), and propolis-B+A (daily oral propolis administration 7 days prior to and 72 h after the ICH induction). Neurocognitive functions of the rats were analyzed using the rotarod challenge and Morris water maze. In addition, the expression of NF-κB, SUR1-TRPM4, MMP-9, and Aquaporin-4 was analyzed using immunohistochemical methods. A TUNEL assay was used to assess the percentage of apoptotic cells. Mannitol significantly improved cognitive–motor functions in the ICH group, evidenced by improved rotarod and Morris water maze completion times, and lowered SUR-1 and Aquaporin-4 levels. It also significantly decreased cerebral edema by day 3. Similarly, propolis treatments (propolis-A and propolis-B+A) showed comparable improvements in these tests and reduced edema. Moreover, combining propolis with mannitol (propolis-M) further enhanced these effects, particularly in reducing edema and the Virchow-Robin space. These findings highlight the potential of propolis from the Indonesian stingless bee, Geniotrigona thoracica, from the Central Tapanuli region as a neuroprotective, adjunctive therapy. [ABSTRACT FROM AUTHOR]

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., (Copyright© Bentham Science Publishers; For any queries, please email at epub@benthamscience.net.)