Hydroxytyrosol protects against acrolein induced preosteoblast cell toxicity: Involvement of Nrf2/Keap1 pathway

• Smoking component acrolein induces oxidative stress in preosteoblast cells.
• Acrolein impairs autophagy and induces mitochondrial accumulation.
• HT activates phase II enzymes through promoting Nrf2 nuclear translocation.
• HT protects preosteoblast cells from acrolein induced mitochondrial dysfunction.

Olive oil, the primary source of dietary fat in the Mediterranean diet, is reported to have benefits on bone health, mechanisms of which remain obscure. Here we investigated the protective effects of hydroxytyrosol (HT), a major polyphenol in olive on preosteoblast toxicity induced by acrolein, the major component of cigarette smoke. Acrolein at 75 µM, induced significant oxidative stress which was attributed to the inhibition of Nrf2 nuclear translocation and suppression of phase II enzymes. And HT could efficiently promote Phase II enzymes activation and prevent the decrease of antioxidative enzymes, protect the autophagy pathway and maintain the normal level of mitochondrial complexes. These results indicated that cigarettes smoking could damage preosteoblast cells by inducing oxidative stress and mitochondrial dysfunction. While through activation of Keap1/Nrf2 pathway, olive component HT could contribute to cellular protection and potential bone health.