Oleuropein

Inhibition of Sirtuin 1 (SIRT1) impairs porcine oocyte maturation and embryonic development. Herein, we investigated whether oleuropein (OLE) restores oocyte quality compromised by the SIRT1 inhibitor EX527. Treatment with EX527 (1 μM) significantly suppressed SIRT1 expression and reduced first polar body extrusion (Control: 74.0 ± 2.8% vs. EX527: 59.9 ± 1.1%, p < 0.001), cleavage rate, blastocyst formation (Control: 43.8 ± 5.4% vs. EX527: 30.4 ± 5.9%, p < 0.05), and cell number. EX527 also induced oxidative stress, as evidenced by increased ROS levels and decreased GSH content, mitochondrial dysfunction (reduced mitochondrial abundance, ATP content, and membrane potential), lipid dysregulation (reduced fatty acids and lipid droplets), and increased apoptosis and autophagy, as indicated by upregulated CB, BAX, ERK1, LC3β, and P62 expression. Co-treatment with OLE (5 μM) significantly restored first polar body extrusion (EX527: 59.4 ± 2.0% vs. EX527 + OLE: 69.7 ± 1.3%, p < 0.001), cleavage rate, blastocyst formation (EX527: 25.3 ± 2.4% vs. EX527 + OLE: 41.7 ± 6.0%, p < 0.01), and cell number. OLE reactivated the SIRT1/NRF2 pathway, improved redox homeostasis (upregulated CAT, SOD1, and SOD2 expression), enhanced mitochondrial biogenesis (increased TFB1M and NRF1 expression), normalised lipid metabolism (upregulated PPARγ, ACACA, and PLIN2), and attenuated aberrant apoptotic and autophagic signalling. The SIRT1 activator resveratrol (2 μM) produced comparable effects. Collectively, these results indicate that OLE mitigates the detrimental effects of SIRT1 inhibition via the SIRT1/NRF2 axis and promotes cytoplasmic maturation, suggesting potential applications in assisted reproduction.

Iron is an essential micronutrient involved in key physiological processes, including oxygen transport and mitochondrial energy production. As humans lack a regulated excretory pathway for excess iron, systemic homeostasis depends on tightly controlled mechanisms of intestinal absorption, cellular storage, and recycling. Dysregulation of these processes may result in iron deficiency or overload, both associated with significant health implications. Plant bioactive compounds, a diverse group of secondary metabolites present in various plant tissues, have gained attention for their modulatory effects on iron metabolism. Emerging evidence suggests that these compounds influence the expression and activity of iron-regulatory proteins such as hepcidin, ferroportin (FPN), ferritin, transferrin, and divalent metal transporter 1 (DMT1). Their biological effects are frequently attributed to antioxidant, metal-chelating, and anti-inflammatory properties. This review provides a comprehensive overview of selected plant-derived bioactive compounds-curcumin, catechins, quercetin, resveratrol, sulforaphane, tannins, myricetin, apigenin, and oleuropein-and their roles in iron metabolism and homeostasis. Special attention is given to their mechanistic actions and therapeutic potential in the context of iron-related disorders.