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作 者:李佳慧 孙健 敖霜 余薇[1] 贲亚琍[1] 张雯[1] 许庆安 LI Jiahui;SUN Jian;AO Shuang;YU Wei;BEN Ya-li;ZHANG Wen;XU Qing-an(Jianghan University,Hubei Wuha 430056,China;Wuhan First Stomatological Hospital,Hubei Wuhan 430022,China.)
机构地区:[1]江汉大学,湖北武汉430056 [2]武汉第一口腔医院,湖北武汉430022
出 处:《临床口腔医学杂志》2023年第5期259-263,共5页Journal of Clinical Stomatology
基 金:国家自然科学基金项目(81570968);江汉大学校级一般项目(2021yb128)。
摘 要:目的:研究二氢杨梅素(dihydromyricetin,DMY)对糖尿病诱导的大鼠牙周牙槽骨吸收的影响及可能的作用机制。方法:使用125、250、500 mg/kg的DMY作用于链脲佐菌素(streptozotocin,STZ)诱导的糖尿病大鼠模型,制取磨牙切片进行数字切片扫描仪,计算破骨细胞数目;大鼠上颌骨进行Micro-CT扫描,分析牙槽骨吸收情况。体外培养MC3T3-E1细胞使用10、20、40μmol/L的DMY处理,MTT法检测细胞活力;体外培养破骨细胞使用10、20、40μmol/L DMY处理,抗酒石酸酸性磷酸酶(TRAP)染色进行破骨细胞观察和计数,ELISA检测促炎细胞因子IL-1β和抗炎细胞因子IL-10。结果:DMY抑制STZ大鼠牙槽骨破骨细胞的生成;缓解STZ大鼠牙槽骨的吸收。体外实验DMY抑制RANKL诱导的破骨细胞的生成,抑制RANKL诱导破骨细胞生成过程中IL-1β的表达。并且10、20、40μmol/L DMY对MC3T3-E1细胞无毒性。结论:DMY通过抑制破骨细胞的生成,减少糖尿病造成的牙槽骨吸收。Objective:To investigate the effect of dihydromyricetin(DMY)on diabetes-induced periodontal alveolar bone resorption in rats and the possible mechanism of action.Methods:DMY at 125,250 and 500 mg/kg was used to act on the streptozotocin(STZ)-induced diabetic rat model,and molar sections were prepared for digital section scanner to calculate the number of osteoclasts.The rat maxilla was scanned by micro-CT to analyze the alveolar bone resorption.MC3T3-E1 cells were cultured in vitro using 10,20 and 40μmol/L DMY treatment and MTT assay for cell viability,cultured osteoblasts were treated with 10,20,40μmol/L DMY,anti-tartrate acid phosphatase(TRAP)staining for osteoblast observation and counting,and ELISA for the pro-inflammatory cytokine IL-1βand the anti-inflammatory cytokine IL-10.Results:DMY inhibited the production of osteoclasts in the alveolar bone of STZ rats,it alleviated the resorption of alveolar bone in STZ rats.In vitro experiment,DMY inhibited RANKL-induced osteoclastogenesis and suppressed IL-1βexpression during RANKL-induced osteoclastogenesis.And 10,20,40μmol/L DMY was not toxic to MC3T3-E1 cells.Conclusion:DMY reduces alveolar bone resorption caused by diabetes by inhibiting the formation of osteoclasts.
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