Gene therapy has emerged as a transformative therapeutic strategy for addressing genetic disorders, refractory cancers, and infectious diseases; however, its clinical translation is significantly hindered by the lack of efficient, safe, and targeted gene delivery vectors. Conventional viral vectors are limited by immune rejection, narrow packaging capacity, and potential biosafety risks, while early nonviral vectors often suffer from poor targeting ability, low intracellular delivery efficiency, and insufficient protection of genetic cargo. Thus, the development of advanced gene delivery vectors is critical to overcoming these bottlenecks, safeguarding the stability and bioavailability of genetic materials, and unlocking the full therapeutic potential of gene-based therapies. Metal-organic frameworks (MOFs) are a new type of porous nanomaterial with substantial potential for use in gene delivery due to their large specific surface area, tunable pore size, good biocompatibility, and low toxicity. Here, we present a comprehensive review of MOF synthesis strategies, gene delivery mechanisms, and associated progress in biomedical applications. Genes can be effectively loaded onto MOFs through pore encapsulation, surface adsorption, covalent binding, and in situ encapsulation. Subsequently, surface functionalization methods are used to achieve precise delivery. In tumor-targeted therapy, MOFs can specifically recognize cancer cells and release genes in response to the microenvironment, thereby significantly inhibiting tumor growth. In the field of immune regulation, MOF multifunctionality supports the codelivery of genes and immune drugs, synergistically enhancing the antitumor immune response. However, challenges remain in the clinical application of MOFs, including insufficient biostability, low intracellular delivery efficiency, and potential toxicity. These challenges are expected to be addressed in the future through the development of new stable MOF materials, the optimization of surface engineering strategies, and the construction of intelligent responsive systems, yielding more precise and efficient gene therapy development.

This study describes the purification and preparation of tricin (5, 7, 4-trihydroxy-3, 5-dimethoxyflavone) from Carex Meyeriana Kunth via adsorption and desorption using macroporous resins and high-performance liquid chromatography. Six resins were tested to evaluate the static adsorption and desorption capacities. The HPD-300 resin was selected as the adsorption material to enrich tricin because of its suitable adsorption and desorption capacities. Adsorption thermodynamics and kinetics were studied on HPD-300 resin, and the results agreed with the Langmuir model and quasi-second-order kinetics model, respectively. The parameters of the dynamic adsorption and desorption tests were then optimized. The purity of tricin increased from 2.6 mg/g to 45.1 mg/g with a recovery yield of 76.4% after purification using HPD-300 resin. Then, Prep-HPLC was used to further purify tricin. The purity of tricin reached 99.4%, with a recovery yield of 78.0% thereafter. Tricin exerts an inhibitory effect on the proliferation of various tumor cells, including gastric cancer SGC-7901 cells. It significantly suppresses cell colony formation while also altering cell cycle progression metabolism by decreasing the proportion of cells in the G₀/G₁ phase and increasing the proportion in the S and G₂/M phases. Additionally, tricin affects the efficiency of SGC-7901 cell lactate production, ATP content, and glucose uptake. These findings suggest that tricin may impede tumor cell proliferation through its impact on cell cycle progression and energy metabolism.

Panaxynol (PAL), a bioactive polyacetylene abundant in dietary plants such as carrots and ginseng, has shown potential in mitigating immune-related diseases, including rheumatoid arthritis (RA). This study investigates the anti-RA effects of PAL through ferroptosis induction and anti-inflammatory mechanisms. In vitro experiments revealed that PAL significantly reduced the viability of collagen-induced arthritis fibroblast-like synoviocytes (CIA-FLS) by triggering ferroptosis, as evidenced by decreased glutathione (GSH) levels, increased lipid peroxidation (LPO) and iron accumulation, and downregulation of key ferroptosis regulators (SLC7A11, GPX4). Furthermore, PAL inhibited the NF-κB pathway, leading to reduced secretion of pro-inflammatory cytokines (TNF-α, IL-1β). In vivo studies using a CIA rat model demonstrated that PAL alleviated joint swelling, reduced the arthritis index, and improved trabecular bone density, highlighting its therapeutic potential. Transcriptomic analysis revealed that PAL modulated ferroptosis and NF-κB signaling through ceRNA networks, with experimental validation confirming the involvement of TFR1 and NIK axes. Notably, inflammatory factors were found to attenuate the sensitivity of CIA-FLS to PAL-induced ferroptosis, suggesting a complex interplay between inflammation and cell death regulation. These findings not only elucidate the mechanism of PAL in RA mitigation but also underscore its potential as a dietary intervention for chronic inflammatory diseases. By integrating traditional dietary knowledge with modern functional food science, this study provides a theoretical basis for the development of functional foods rich in PAL to support joint health.

The objective of this study was to enhance the membrane permeability and anticancer effectiveness of (20S)-protopanaxadiol (PPD) by introducing triphenylphosphonium into the OH group at the C-3 site. This study shows that the anti-proliferation activity of CTPPPPD, with an IC50 value of 1.65 ± 0.10 μmol/L, was 33-times better than that of PPD (with an IC50 value of 54.56 ± 4.56 μmol/L) and superior to that of cisplatin (with an IC50 value of 1.82 ± 0.25 μmol/L) against A549 cells. Biological examinations suggested that CTPPPPD treatment reduced the growth rate of A549 cells, increased the permeability of cell membranes, and changed the structure of chromosomal DNA in a concentration-dependent manner. Annexin V/PI assay and flow cytometry were employed to detect the effect of CTPPPPD on the apoptosis of A549 cells. The results showed that CTPPPPD could induce the apoptosis of A549 cells, and the apoptosis rate of A549 cells treated with 0, 1.0, 2.0, and 4.0 μM of CTPPPPD for 24 h was 0%, 4.9%, 12.7%, and 31.0%, respectively. The integration of transcriptomics and metabolomics provided a systematic and detailed perspective on the induced antitumor mechanisms. A combined analysis of DEGs and DAMs suggested that they were primarily involved in the central carbon metabolism pathway in cancer, as well as the metabolism of aminoacyl-tRNA biosynthesis, alanine, aspartate, and glutamate. Central carbon metabolism in cancer-related genes, i.e., SLC16A3, FGFR3, LDHA, PGAM1, and SLC2A1, significantly reduced after treatment with CTPPPPD. In particular, the dominant mechanism responsible for total antitumor activity may be attributed to perturbations in the PI3K-AKT, MAPK, and P53 pathways. The findings derived from transcriptomics and metabolomics were empirically confirmed through q-PCR and molecular docking. Further analyses revealed that CTPPPPD could be a promising lead for the development of protopanaxadiol for non-small-cell lung cancer (NSCLC) drugs.