ABSTRACT
PURPOSE: To investigate the effect of Morinda officinalis polysaccharides(MOP) on the expression of fibronectin(FN) and fibronectin containing extra domain A(FN-EDA) in inflammatory periodontal ligament fibroblasts. METHODS: Thirty six rats were randomly divided into a control group(n=12) and a model group (n=24). The model group used orthodontic wire ligation to establish periodontitis. After three weeks, 6 rats from each group were selected and confirmed by Micro-CT to complete the modeling. The remaining rats in the model group were randomly divided into periodontitis group, normal saline(NS) group, and MOP group. In the MOP group, MOP (200 mg/kg for 3 d, 50 µL for 4 weeks) was injected into the palatal side of the left maxillary first molar of the rats. In the NS group, same volume of NS was injected, and no treatment was performed in the periodontitis group. The left maxillary tissue of rats were taken and the pathological changes of periodontal tissue were observed by H-E staining. The expression of FN and FN-EDA was detected by immunohistochemistry. Periodontal ligament fibroblasts were cultured in vitro, the effect of MOP on cell activity detected by CCK-8. The fourth generation cells were divided into control group, inflammation group (10 mg/mL lipopolysaccharide), and experimental group (12.5 µg/mL MOP, 12.5 µg/mL MOP+10 mg/mL lipopolysaccharide). The expression of FN and FN-EDA was detected by qRT-PCR and Western blot. The data were statistically analyzed using Prism 8.0 software package. RESULTS: In vivo experiments, the expression of FN-EDA in the MOP group was significantly lower than that in the periodontitis group and NS group(Pï¼0.05), and the infiltration of inflammatory cells was reduced. However, there was no significant difference in the expression of FN in each group. In vitro experiments, compared with the control group, the expression of FN-EDA mRNA and protein in the inflammation group was significantly increased(Pï¼0.000 1). MOP significantly reduced the expression of FN-EDA in inflammatory cells, but had no significant effect on FN expression. CONCLUSIONS: With increased expression of FN-EDA in inflammatory periodontal ligament tissues and cells, MOP may play a role in inhibiting inflammation by down-regulating FN-EDA.
Subject(s)
Fibroblasts , Fibronectins , Morinda , Periodontal Ligament , Polysaccharides , Animals , Fibroblasts/drug effects , Fibroblasts/metabolism , Polysaccharides/pharmacology , Periodontal Ligament/drug effects , Periodontal Ligament/metabolism , Periodontal Ligament/cytology , Rats , Morinda/chemistry , Fibronectins/metabolism , Fibronectins/genetics , Periodontitis/drug therapy , Periodontitis/metabolism , Inflammation/drug therapy , Rats, Sprague-DawleyABSTRACT
PURPOSE: The purpose of this study was to investigate the relationship of IL-1beta expressed in buccal cells and the polymorphisms of IL-1beta(+3953) with chronic periodontitis. METHODS: Thirty-six patients with different severity of periodontal disease and thirty-six subjects with healthy periodontal tissues participated in this study. Buccal cells and peripheral venous blood samples were collected and the periodontal status were recorded. Immunohistochemical analysis of IL-1beta expressed in buccal cells was carried out and the polymorphisms in IL-1beta(+3953) were analyzed by polymerase chain reaction-restriction fragment length polymorphism after extracting DNA from peripheral venous blood. Then the differences in the level of IL-1beta expressed in buccal cells and the distribution of each genotype in IL-1beta(+3953) were compared. Multiple linear regression was used to correlate the periodontal status with the polymorphisms in IL-1beta(+3953) and the expression of IL-1beta) in buccal cells. RESULTS: The carrying ratio of IL-1beta(+3953) allel II in severe chronic periodontitis (12%) was significantly higher than the healthy control group(0). The level of IL-1beta expressed in buccal cells of patients with chronic periodontitis was also significantly higher than that of subjects with healthy periodontal conditions (chi2 = 365.095, P < 0.001). Clinical attachment loss and probing depth correlated positively with the expression of IL-1beta (CAL, P < 0.05; PD, P < 0.01) and no correlation was found between plaque index, bleeding on probing,the polymorphisms in IL-1beta(+3959) and the levels of IL-1beta. CONCLUSIONS: The results of this small sample study suggested that the level of IL-1beta expressed in buccal cells showed the severity of chronic periodontitis and the IL-1beta(+3953) genotype did not make the level of IL-1beta expressed in buccal cells changed significantly.
