Protective effect of catalpol on nicotine‑induced injury of alveolar bone and associated underlying mechanisms.

Smoking is an important factor that causes periodontitis, which manifests as alveolar bone injury and absorption, and has a high incidence and unfavorable treatment efficacy. Nicotine causes ischemia and inflammation of the periodontium and inhibits the mineralization of alveolar bones. Previous studies have revealed the anti‑tumor biological activities of catalpol, in addition to neuroprotection and anti‑inflammation. The present study therefore investigated the underlying protective mechanism of catalpol in alveolar bone injury. A total of 24 Wistar rats were infused with nicotine (0.7 mg/kg for 30 days), followed by subcutaneous injection of catalpol (2 µg/kg for 14 days). The loss of alveolar bone was examined, and bone alkaline phosphatase (AP) and osteocalcin levels were examined by ELISA. The expression of tumor necrosis factor (TNF)‑α and cyclooxygenase‑2 (COX‑2) was quantified by reverse transcription‑quantitative polymerase chain reaction analysis and western blotting. Treatment with nicotine decreased AP and osteocalcin levels, increased TNF‑α and COX‑2 expression levels, and led to alveolar bone loss compared with the control group. Catalpol decreased bone loss, increased AP and osteocalcin, and decreased TNF‑α and COX‑2 expression compared with the nicotine treatment group. Catalpol may alleviate nicotine‑induced injury and alveolar bone loss via inhibition of inflammatory factors, and facilitate the mineralization of alveolar bones.