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


Bayraktaroglu S. B., TASLI P. N., Can B., Özkan F., Temizkan İ., Bayraktar E., ...Daha Fazla

Journal of Trace Elements in Medicine and Biology, cilt.94, 2026 (SCI-Expanded, Scopus) identifier identifier

  • Yayın Türü: Makale / Tam Makale
  • Cilt numarası: 94
  • Basım Tarihi: 2026
  • Doi Numarası: 10.1016/j.jtemb.2026.127847
  • Dergi Adı: Journal of Trace Elements in Medicine and Biology
  • Derginin Tarandığı İndeksler: Science Citation Index Expanded (SCI-EXPANDED), Scopus, BIOSIS, EMBASE, MEDLINE
  • Anahtar Kelimeler: Aging, Anti-Aging, Boron, D-Galactose, Inflammaging, Inflammation, ROS
  • Dokuz Eylül Üniversitesi Adresli: Evet

Özet

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.