Impact of Sulfate-Arsenical-Ferruginous Water on Apoptosis, Oxidative Stress, and Gene Expression of Inflammatory Mediators and MicroRNA in Human Osteoarthritic Chondrocytes Stimulated by IL-1β - Report - MDSpire
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Impact of Sulfate-Arsenical-Ferruginous Water on Apoptosis, Oxidative Stress, and Gene Expression of Inflammatory Mediators and MicroRNA in Human Osteoarthritic Chondrocytes Stimulated by IL-1β
Impact of Sulfate-Arsenical-Ferruginous Water on Osteoarthritic Chondrocytes
Overview
This study evaluates the effects of sulfate-arsenical-ferruginous Levico water on apoptosis, oxidative stress, and gene expression in human osteoarthritic chondrocytes. Findings indicate that Levico water can counteract IL-1β-induced damage and modulate inflammatory pathways.
Background
Osteoarthritis (OA) is a prevalent chronic musculoskeletal disorder characterized by cartilage degeneration and inflammation. Balneotherapy, particularly with mineral waters like sulfate-arsenical-ferruginous Levico water, has shown potential benefits in managing OA symptoms. Understanding the biological mechanisms of such treatments can enhance therapeutic strategies for OA management.
Levico water (LW) at 50% and 25% concentrations improved cell viability and reduced apoptosis in IL-1β stimulated chondrocytes.
LW treatment significantly inhibited the expression of pro-inflammatory cytokines such as IL-1β, IL-6, and TNF-α.
Gene expression of matrix metalloproteinases (MMPs) 1 and 13 was reduced following LW treatment.
LW upregulated miR-140 and downregulated miR-34a and miR-181a in IL-1β stimulated cells.
Pre-incubation with BAY 11–7082 enhanced the protective effects of LW against IL-1β damage.
Clinical Implications
The findings suggest that sulfate-arsenical-ferruginous water may serve as a complementary treatment for osteoarthritis, potentially reducing inflammation and apoptosis in chondrocytes. Clinicians may consider incorporating balneotherapy into comprehensive OA management strategies.
Conclusion
Sulfate-arsenical-ferruginous Levico water demonstrates significant potential in modulating key pathological processes in osteoarthritis, warranting further exploration in clinical settings.