RESUMEN
Background and purpose: Scientific research is crucial to develop therapies for various disease severity levels, as modern drugs cause side effects and are difficult to predict. Researchers are exploring herbal alternatives with fewer side effects, particularly propolis, which has been validated through in vitro, in vivo, and clinical studies. This will focus on scientific evidence and its supporting technology for developing new bioactive compounds for chronic diseases. Nanotechnology can improve the delivery and absorption of herbal medicines, which often have poor bioavailability due to their high molecular weight and solubility in water, particularly in oral medicines. This technology can enhance propolis's effects through multi-target therapy and reduce side effects. Experimental approach: All publications related to each section of this review were discovered using the search engines Google Scholar, Scopus, and Pubmed. This was only available for publication between 2013 and 2023. The selected publications were used as references in this review after being thoroughly studied. Key results: Evaluation of propolis active compounds, the classification of propolis nano formulations, design concepts, and mechanisms of action of propolis nano formulation. Additionally, the challenges and prospects for how these insights can be translated into clinical benefits are discussed. Conclusion: In the last ten years, a list of nanoformulation propolis has been reported. This review concludes the difficulties encountered in developing large-scale nanoformulations. To commercialize them, improvements in nano carrier synthesis, standardized evaluation methodology within the framework of strategy process improvement, and Good Manufacturing Practices would be required.
RESUMEN
Cirrhosis naturally progresses through three stages: compensated, decompensated, and late decompensated, which carry an elevated risk of death. Although curcumin's anti-cirrhosis effects have been studied, underlying mechanism in preventing cirrhosis progression and the correlation between curcumin's action with upregulated genes remains insufficiently explored. In this study, we employed network pharmacology approach to construct a drug-target-disease network through bioinformatics and validate the findings with molecular docking and dynamic simulation. The curcumin-targeted liver cirrhosis network encompassed 54 nodes with 282 edges in protein-protein interactions (PPI) network. By utilizing network centrality analysis, we identified eight crucial genes. KEGG enrichment pathway revealed that these crucial genes are involved in pathway of cancer, endocrine resistance, estrogen signaling, chemical carcinogenesis-receptor activation, lipid metabolism, and atherosclerosis. Notably, these eight genes predominantly participate in cancer-related pathways. Further investigation revealed upregulation of four genes and downregulation of four others in hepatocellular carcinoma patients. These upregulated genes-MAPK8, SRC, PPARG, and HSP90AA1-strongly correlated with reduced survival probability in liver hepatocellular carcinoma patients with survival times approximately under 4000 days (â¼11 years). Molecular docking and molecular dynamic results exhibited curcumin's superior binding affinities and stability compared to native ligands of MAPK8, SRC, PPARG, and HSP90AA1 within 50 ns simulations. Moreover, MM-GBSA analysis showed stronger binding energy of curcumin to MAPK8, SRC, and HSP90AA1 than native ligand. In conclusion, this study provides valuable insights into curcumin's potential mechanisms in preventing liver cirrhosis progression, specifically in HCC. These findings offer a theoretical basis for further pharmacological research into anti-HCC effect of curcumin.Communicated by Ramaswamy H. Sarma.
RESUMEN
BACKGROUND: Cardol is a major bioactive constituent in the Trigona incisa propolis from Indonesia, with a strong in vitro antiproliferative activity against the SW620 colorectal adenocarcinoma cell line (IC50 of 4.51 ± 0.76 µg/mL). Cardol induced G0/G1 cell cycle arrest and apoptotic cell death. The present study was designed to reveal the mechanism of cardol's antiproliferative effect and induction of apoptosis. METHODS: Changes in cell morphology were observed by light microscopy. To determine whether the mitochondrial apoptotic pathway was involved in cell death, caspase-3 and caspase-9 activities, western blot analysis, mitochondrial membrane potential, and intracellular reactive oxygen species (ROS) levels were assayed. RESULTS: Changes in the cell morphology and the significantly increased caspase-3 and caspase-9 activities, plus the cleavage of pro-caspase-3, pro-caspase-9 and PARP, supported that cardol caused apoptosis in SW620 cells within 2 h after treatment by cardol. In addition, cardol decreased the mitochondrial membrane potential while increasing the intracellular ROS levels in a time- and dose-dependent manner. Antioxidant treatment supported that the cardol-induced cell death was dependent on ROS production. CONCLUSION: Cardol induced cell death in SW620 cells was mediated by oxidative stress elevation and the mitochondrial apoptotic pathway, and these could be the potential molecular mechanism for the antiproliferative effect of cardol.
