Sodium pentaborate pentahydrate ameliorates inflammaging-like phenotypes by modulating redox status in a D-galactose-induced accelerated aging rat model.

Abstract

Boron is a bioactive trace element that influences cellular signaling by forming ester complexes with ribose-containing molecules, such as NAD and S-adenosylmethionine. Age associated chronic low-grade inflammation ('inflammaging') and oxidative stress are pivotal contributors to functional decline. In this study, we evaluated the potential of sodium pentaborate pentahydrate (NaB) to mitigate accelerated aging-like phenotypes in a D-galactose (D-gal) rat model. Male Sprague-Dawley rats received D-gal (1000 mg/kg/day, subcutaneous) for 8 weeks to induce an oxidative dominant accelerated aging phenotype, followed by weight adjusted NaB (100 µg/kg/day, subcutaneous) or vehicle for 4 weeks. Multi organ endpoints included cognitive/locomotor assessments (NOR and open-field), histology, oxidative stress markers (ROS, CAT, GST), inflammatory cytokines, and senescence associated readouts (p16/p21, lipofuscin, and global DNA methylation). NaB administration improved recognition memory, reduced systemic ROS levels, restored antioxidant enzyme activity, and shifted cytokine profiles toward a less pro-inflammatory state. Furthermore, NaB attenuated senescence associated markers and partially normalized fatty acid composition in the brain and liver. As specific pathway level mediators (e.g., Nrf2/SIRT1 or NF-κB) were not directly quantified, these findings are interpreted as hypotheses consistent with the observed redox and cytokine modulations rather than definitive causal proof. While these results provide a preclinical proof-of-concept for the amelioration of D-galactose-induced aging-like phenotypes, further investigations are warranted to evaluate the safety and efficacy of boron-based interventions in broader physiological contexts.