ナトリウムペンタボレートペンタハイドレートは、D-ガラクトース誘発性加速老化ラットモデルにおいてレドックス状態を調節することにより、炎症老化様表現型を改善する

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.