Osteoarthritis (OA) is a prevalent joint disorder marked primarily by the progressive breakdown of articular cartilage. Pyroptosis, an inflammatory programmed cell death mechanism, exacerbates OA progression. Ginsenoside Rh2 (Rh2), a bioactive compound derived from traditional Chinese medicine, has shown potential therapeutic effects in OA. However, its underlying molecular mechanisms in OA treatment remain to be fully elucidated. To investigate the therapeutic potential of Rh2, an in vitro OA model was generated via LPS treatment of human chondrocytes (C-28/I2). The anti-inflammatory and anti-pyroptotic properties of Rh2 were subsequently assessed by quantifying the levels of key inflammatory cytokines using ELISA, immunofluorescence assessment of extracellular matrix components, Western blot analysis of pyroptosis-related proteins, and LDH release assays. The interaction between Rh2 and platelet-activating factor receptor (PAFR) was verified using molecular docking and cellular thermal shift assay (CETSA). Finally, functional validation of Rh2's target specificity was achieved through transfection of PAFR overexpression or knockdown plasmids into chondrocytes. In the chondrocyte OA model, Rh2 treatment significantly suppressed PAFR expression and inhibited the NF-κB signaling pathway, resulting in the significant downregulation of key pyroptosis-related proteins, including NLRP3, cleaved Caspase-1, and GSDMD-N, as well as a decrease in the secretion of pro-inflammatory cytokines IL-1β and IL-18. These effects collectively attenuated chondrocyte pyroptosis and protected cartilage cells. Conversely, PAFR overexpression completely abolished the protective effects of Rh2, demonstrating the critical role of PAFR in mediating Rh2's therapeutic actions. Using a human chondrocyte cell line (C-28/I2) and focusing on PAFR as the target gene, our findings demonstrate that Rh2 alleviates chondrocyte pyroptosis in vitro by specifically targeting PAFR to suppress NF-κB signaling. These results provide a mechanistic basis for further investigation of Rh2 in more complex OA models. The PAFR/NF-κB axis represents a candidate pathway for cartilage protection.

Acidic soils (pH < 5.5) contain elevated levels of phytotoxic aluminum (Al3+) and iron (Fe2+/Fe3+); however, the mechanisms underlying plant adaptation to their coexistence remain poorly understood. Commelina communis, an invasive weed prevalent on acid soils of tea gardens, was exposed to Al (50 and 100 µM) and Fe (100 µM), individually and in combination (pH 4.0), for four weeks. Plant biomass remained unaffected under single or combined stress, accompanied by reciprocal reductions in foliar metal concentrations. However, chlorosis, reduced photosynthetic pigments, and altered photochemical parameters indicated exacerbated chloroplast damage under combined Al and Fe toxicity. Conversely, phenolic and anthocyanin contents in leaves and oxalate in roots peaked under dual stress, coinciding with significantly reduced stress markers. Histochemical analysis revealed that Al3+ and Fe2+ mutually inhibited binding to root tips, reducing membrane injury under co-treatment. Fourier-transform infrared (FTIR) spectroscopy of root tissues showed substantial decreases in cell wall-associated pectin and hemicellulose under Al stress, excess Fe and co-exposure, potentially limiting Al3+ and Fe2+/Fe3+ binding and mitigating rhizotoxic effects. Al treatment alone suppressed malate and citrate exudation, whereas Fe toxicity increased their release. In contrast, oxalate and phenolics exudation were enhanced by Al and Fe, with maximum excretion under combined exposure. These findings reveal two interaction patterns: additive toxicity affecting chloroplast function, and synergistic enhancement of internal and rhizosphere-based detoxification. Taken together, these findings explain the robust spread of C. communis in acid soils, provide a framework for future research on metal co-tolerance, and may inform acid soil management strategies and the development of stress-resilient cultivars.

The purpose the experiment was to investigate the microstructure, localization, and content of silicon inclusions in the leaf epidermis of Quercus robur trees grown in forest-steppe zones of southern Ukraine with varying levels of solar radiation (sunlight intensities). The investigations utilized the electron microscopic method and laser confocal microscopy. It was determined that sunlight intensity influenced size and area of the leaves, leaf epidermis ultrastructure, and change in silicon content in epidermis of Q. robur leaves. The research indicated that trichomes, stomata, and ordinary epidermal cells of oak leaves were the primary accumulators of silicon. The results suggest that variations in the leaf size, microstructure and silicon content contribute to the optimal ability to absorb and reflect light on the leaf surface. These changes may be considered as indicators of plant phenotype plasticity and adaptive markers depending on light intensity conditions. The various compounds of these leaves, including of presence of wax structures and silicon, can be used for practical applications.

IGFBP4 is essential for adipogenesis and is highly expressed in adipocytes and osteoblasts of mice. However, its role in bovine adipogenesis, especially intramuscular adipogenesis, remains unknown. Here, we cloned the CDS of IGFBP4 from Qinchuan cattle and analyzed its protein structure and function. We measured its expression levels in various tissues. The CDS region of the bovine IGFBP4 gene was 777bp long, encoding a protein of 259 amino acids. The in-silico analysis revealed sequence conservation of Bos mutus and Bos indicus, while variation was found in Mus musculus and Rattus norvegicus sequences. The physical and chemical properties of the IGFBP4 protein exhibited an isoelectric point of 7.10 and a molecular mass of 27.89kDa. The protein was predicted to be hydrophilic and lacked a transmembrane structure, with potential phosphorylation and glycosylation sites. Interaction analysis suggested associations with several other proteins. Regarding tissue expression, the mRNA level of the IGFBP4 gene was highest in the liver, lowest in muscle, and significantly higher in subcutaneous fat compared to intramuscular fat in Qinchuan beef cattle. These findings indicate a potential role of theIGFBP4 gene in regulating bovine adipogenesis and lipid metabolism. This study provides a foundation for exploring the underlying molecular mechanism of intramuscular fat deposition in cattle.

Water loss is a major challenge for photosynthetic organisms. Most are prone to drought stress and only few can tolerate full desiccation. Here, we investigated regulation of photosynthetic electron flow during dehydration and rehydration in Haematococcus lacustris, a desiccation tolerant green alga. During dehydration, non-photochemical quenching (NPQ) increased for dissipating excess light energy, while light-use efficiency of photosystems II (PSII) and I (PSI) decreased. The reaction centre of PSI (P700) became electron-limited at its donor side, helping form photoprotective P700+. Inhibiting alternative oxidases with octyl gallate delayed chlorophyll fluorescence quenching, indicating that plastid terminal oxidases (PTOX) supported formation of NPQ during desiccation. Reduction rates of P700+ during a saturating pulse were slower if cells dehydrated slower, showing that photoprotection was upregulated during desiccation acclimation. During rehydration, octyl gallate and diphenyleneiodonium (DPI), a flavoenzyme inhibitor, slowed oxidation of P700 under actinic light, indicating PTOX and flavodiiron proteins (FLV) were involved in maintaining P700+. A similar response occurred with the protonophore nigericin. We conclude that beyond preventing over-reduction of the electron transport chain, PTOX and FLV facilitated thylakoid luminal acidification under low water stress, protecting photosystems via NPQ, photosynthetic control and P700+ formation.