D-galactose-induced aging and obese conditions contribute to aging and pathologies in dental pulp of male wistar rats

Abstract

Our previous studies demonstrated that both D-galactose (D-gal)-mediated aging and high-fat diet (HF)-promoted obesity trigger inflammation, impair mitochondrial function in heart and brain, and disrupt bone homeostasis. However, the dental pulp pathologies in aging and obesity remain unclear. Insight into pulp biology under systemic conditions may facilitate strategies for maintaining pulp vitality. This study explored the effects of D-gal-mediated aging and HF-promoted obesity and co-administered conditions on aging, inflammation, oxidative stress, mitochondrial dynamics, and cell death in rats' dental pulp. Forty-eight male Wistar rats were randomly allocated to normal diet (ND) or HF. At week 13, each dietary condition was subdivided into four subgroups (n = 6/subgroup). Each subgroup was administered either vehicle (NDV or HFV; 0.9 % normal saline, subcutaneous injection, once daily) or D-gal (NDD or HFD; 150 mg/kg/day, subcutaneous injection, once daily) for four or eight weeks. After euthanasia, rats' dental pulp was gathered. At both time points, HF-fed rats showed insulin-resistance and hypercholesterolemia; D-gal caused only insulin-resistance in ND-fed rats and did not exacerbate metabolic disorder in HF-fed rats. At four weeks, pulpal inflammation was observed in the HFD rats. At eight weeks, dental pulp from NDD and HFV rats exhibited senescence and inflammation, while HFV rats also showed impaired mitophagy and increased apoptosis. The pulpal pathologies were most observed in eight-week HFD rats including senescence, inflammation, oxidative stress, imbalanced mitochondrial dynamics, impaired mitophagy and autophagy, and increased apoptosis. These findings suggest D-gal-mediated aging aggravated senescence and pathologies in dental pulp of obese rats progressively over time.