Imbalanced and Unchecked: The Role of Metal Dyshomeostasis in Driving COPD Progression.

Chronic obstructive pulmonary disease (COPD) is a chronic respiratory condition characterized by persistent inflammation and oxidative stress, which ultimately leads to progressive restriction of airflow. Extensive research findings have cogently suggested that the dysregulation of essential transition metal ions, notably iron, copper, and zinc, stands as a critical nexus in the perpetuation of inflammatory processes and oxidative damage within the lungs of COPD patients. Unraveling the intricate interplay between metal homeostasis, oxidative stress, and inflammatory signaling is of paramount importance in unraveling the intricacies of COPD pathogenesis. This comprehensive review aims to examine the current literature on the sources, regulation, and mechanisms by which metal dyshomeostasis contributes to COPD progression. We specifically focus on iron, copper, and zinc, given their well-characterized roles in orchestrating cytokine production, immune cell function, antioxidant depletion, and matrix remodeling. Despite the limited number of clinical trials investigating metal modulation in COPD, the advent of emerging methodologies tailored to monitor metal fluxes and gauge responses to chelation and supplementation hold great promise in unlocking the potential of metal-based interventions. We conclude that targeted restoration of metal homeostasis represents a promising frontier for ameliorating pathological processes driving COPD progression.

Protective effect of hydroxysafflor yellow A on MSCs against senescence induced by d-galactose.

Objective: To examine the protective effects of hydroxysafflor yellow A (HSYA) against the senescence of mesenchymal stem cells (MSCs) induced by d-galactose (d-gal) in vitro, and investigate the potential mechanism involved. Methods: Grouping experiment, Normal control (NC) group: conventional culture with complete medium; Senescence group: MSCs were cultured for 48 h with complete medium containing 10 g/L d-gal; HSYA group: on the basis of senescence induction, HSYA with the suitable concentration was used to protect MSCs. The key experimental indices associated with oxidative stress, inflammatory response, cell senescence, proliferation and apoptosis were measured through chemical colorimetry, ß-galactosidase staining, EdU incorporation and flow cytometry, respectively. The relative quantity (RQ) of proteins related closely to cell proliferation, apoptosis, and NF-κB signaling were measured by Western blotting. Results: As compared with Senescence group, treatment with HSYA (120 mg/L) effectively ameliorated the adverse situation of MSCs. Oxidation stress and inflammation along with d-Gal induction was dramatically alleviated in MSCs; The ß-Gal-positive staining indicated that MSC senescence was significantly mitigated; The proliferative capability of MSCs was significantly increased by up-regulating PCNA and inhibiting p16 expression; The anti-apoptotic effect on MSCs was exerted by down-regulating the RQ of cleaved Caspase-3 and Bax; The activity of NF-κB signaling in MSCs was notably suppressed through inhibiting phosphorylation of IKKß and p65. Conclusion: HSYA (120 mg/L) significantly delayed the d-Gal-induced senescence process in MSCs through attenuating inflammatory reaction and oxidative stress, and suppressing the activity of NF-κB signaling.