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

Abstract

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.