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.

Nicotine in Inflammatory Diseases: Anti-Inflammatory and Pro-Inflammatory Effects

“…In an in vivo study, 5-week-old male Wistar rats intraperitoneally injected with nicotine (0.7 mg/kg for 30 days) exhibited decreased levels of bone alkaline phosphatase and osteocalcin as important markers for bone mineralization and activity of osteoblasts, with increased TNF-a and COX−2 expression levels causing ischemia and inflammation of the periodontium and higher alveolar bone loss. Here catalpol was shown to improve nicotine-induced injury to the alveolar bone by promoting alveolar bone mineralization and inhibiting the inflammatory factors (75). Another in vivo study on periodontitis-susceptible Fischer 344 rats injected with nicotine in the neck skin (0.8 mg/kg for 3 weeks) and intraperitoneally injected with LPS (100 mg/kg) found that these developed significantly more periodontal bone loss and periodontal tissue destruction, while nAChR antagonist mecamylamine abolished this effect.…”

Catalpol protects against 2,3,7,8‐tetrachlorodibenzo‐p‐dioxin‐induced cytotoxicity in osteoblastic MC3T3‐E1 cells

“…Catalpol increases the bone healing capacity of bone marrow mesenchymal stem cells in a rat model of critical-sized calvarial defects and attenuates bone loss in a rat model of ovariectomy (Zhu, Wang, Jia, Xu, & Chai, 2019). Furthermore, catalpol may alleviate nicotine-induced injuries and alveolar bone loss via the inhibition of inflammatory factors, as well as facilitate the mineralization of alveolar bones (Li, Jin, & Mao, 2017). Lai et al (2015) demonstrated that catalpol alleviates bone loss induced by estrogen deficiency by regulating T-helper 1/2 cells in ovariectomized mice.…”

Prognostic Factors of Grade 2-3 Endo-Periodontal Lesions Treated Nonsurgically in Patients with Periodontitis: A Retrospective Case-Control Study

“…Second, periodontal tissue is rich in blood vessels, but the nicotine in cigarettes constricts the blood vessels, affecting circulation around the periodontal tissue and inhibiting its metabolism [38]. ird, smoking affects the differentiation and attachment of periodontal fibroblasts as well as osteoblast activity, which can inhibit new alveolar bone attachment formation and regeneration [39,40]. Moreover, smoking can increase the risk of losing endodontically treated teeth [19] and has been reported as a significant prognostic factor for developing apical periodontitis [41].…”