Mechanism Underlying Carvacrol-induced Alveolar Bone Repair via the Phosphatidylinositol 3-kinase Pathway in Periodontal Disease
Nian TengiD, Zhaoxun LiiD, Tiantian GaoiD, Xiang Yanrui, Zhou Lulu, Gao Xiang
Abstract
BackgroundConventional antibiotic treatments do not restore the structure of periodontal tissues and can cause antibiotic resistance. This study describes the mechanism by which carvacrol regulates alveolar bone osteoblasts in periodontal disease. MethodsA rat model of periodontal disease (P group) was created by ligating the first molar and injecting lipopolysaccharide (LPS). Additionally, a control model (C group) was created. The treatment models received low (L group), medium (M group), and high (H group) doses of carvacrol hydrogel. In vitro, rat osteoblast cells were divided into the C, P, L, M, H, and carvacrol + LY294002 (Car+LY group) groups. Immunohistochemical staining analyzed collagen type I and runt-related transcription factor 2 expressions. Western blot analysis detected the phosphatidylinositol 3-kinase (PI3K)/protein kinase B (AKT)/glycogen synthase kinase 3 beta (GSK-3{beta}) pathway-related and osteoblastic proteins. Quantitative reverse transcription polymerase chain reaction measured the expression of inflammatory factors and osteoblastic proteins. The alkaline phosphatase (ALP) colorimetric kit and Alizarin Red S staining kit assessed the osteogenic ability. Detect the expression of COL1 in osteoblasts by immunofluorescence (IF). Transmission electron microscopy detected cell apoptosis. ResultsCarvacrol hydrogel alleviated periodontal symptoms, upregulated PI3K/AKT/GSK-3{beta} pathway-related and osteoblastic proteins, and increased ALP expression and calcified nodules. However, it decreased cell apoptosis and inflammatory factors. LY294002 inhibited the PI3K/AKT pathway and decreased osteoblastic protein expression, ALP coloration, and calcified nodules. ConclusionCarvacrol hydrogel promotes the proliferation and differentiation of alveolar bone osteoblasts by activating the PI3K pathway and inhibiting inflammation-induced bone resorption. This study emphasizes the potential of carvacrol for treating periodontal diseases.
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