Abstract：
OBJECTIVE: To investigate the therapeutic effect of atorvastatin on alveolar bone defect model in rats, and to observe the effect of atorvastatin on Wnt/β-catenin.
METHODS: Thirty rats were randomly divided into normal group (group N), model group (group M) and atorvastatin administration group (group ATV). Except group N, bone defects were made in other rats\' alveolar bone to construct alveolar bone defect model. After successful modeling, 20 mg/kg atorvastatin suspension was administered by gavage in group ATV, and the same amount of sodium carboxymethyl cellulose solution was administered by gavage in group N and group M for twenty-one days. After the last administration, tail vein blood was collected to detect the concentrations of serum osteoprotegerin (OPG), alkaline phosphatase (ALP) and osteocalcin (BPG). H-E staining was used to observe the pathological changes of maxillary defect area, and lane Sandhu score was performed. Tartrate resistant acid phosphatase(TRAP) staining was used to detect the number of osteoclasts in the defect area. Real time fluorescence quantitative PCR(RT-qPCR) and Western blot(WB) were used to detect Wnt, β-catenin and Runx2 mRNA protein expression. Statistical analysis was performed with SPSS 23.0 software package.
RESULTS: Compared with group N, the concentrations of OPG, ALP, BGP and Lane Sandhu score in group M decreased, and the number of osteoclasts increased. Compared with group M, the concentrations of OPG, ALP and BGP and lane Sandhu score in group ATV increased, and the number of osteoclasts decreased. After H-E staining, the amount of bone formation in maxillary defect area in group N was more,there was fewer bone tissues in the defect area in group M, the amount of bone tissues in the defect area increased in group ATV. Compared with group N, Wnt, β-catenin and Runx2 mRNA protein decreased. Compared with group M, Wnt, β-catenin and Runx2 mRNA protein expression increased.
CONCLUSIONS: Atorvastatin can promote the healing of alveolar bone defect and accelerate bone reconstruction in rat models. This effect may be related to the activation of Wnt/β-catenin signaling pathway.
METHODS: Thirty rats were randomly divided into normal group (group N), model group (group M) and atorvastatin administration group (group ATV). Except group N, bone defects were made in other rats\' alveolar bone to construct alveolar bone defect model. After successful modeling, 20 mg/kg atorvastatin suspension was administered by gavage in group ATV, and the same amount of sodium carboxymethyl cellulose solution was administered by gavage in group N and group M for twenty-one days. After the last administration, tail vein blood was collected to detect the concentrations of serum osteoprotegerin (OPG), alkaline phosphatase (ALP) and osteocalcin (BPG). H-E staining was used to observe the pathological changes of maxillary defect area, and lane Sandhu score was performed. Tartrate resistant acid phosphatase(TRAP) staining was used to detect the number of osteoclasts in the defect area. Real time fluorescence quantitative PCR(RT-qPCR) and Western blot(WB) were used to detect Wnt, β-catenin and Runx2 mRNA protein expression. Statistical analysis was performed with SPSS 23.0 software package.
RESULTS: Compared with group N, the concentrations of OPG, ALP, BGP and Lane Sandhu score in group M decreased, and the number of osteoclasts increased. Compared with group M, the concentrations of OPG, ALP and BGP and lane Sandhu score in group ATV increased, and the number of osteoclasts decreased. After H-E staining, the amount of bone formation in maxillary defect area in group N was more,there was fewer bone tissues in the defect area in group M, the amount of bone tissues in the defect area increased in group ATV. Compared with group N, Wnt, β-catenin and Runx2 mRNA protein decreased. Compared with group M, Wnt, β-catenin and Runx2 mRNA protein expression increased.
CONCLUSIONS: Atorvastatin can promote the healing of alveolar bone defect and accelerate bone reconstruction in rat models. This effect may be related to the activation of Wnt/β-catenin signaling pathway.
摘要：
目的：观察阿托伐他汀对大鼠牙槽骨缺损模型的治疗作用。观察阿托伐他汀对Wnt/β-catenin的影响。
方法:30只大鼠随机分为正常组(N组),模型组(M组)和阿托伐他汀给药组(ATV组)。除N组外,在其他大鼠牙槽骨中制作骨缺损，以构建牙槽骨缺损模型。建模成功后,ATV组20mg/kg阿托伐他汀混悬液灌胃给药,N组和M组灌胃给予等量的羧甲基纤维素钠溶液21天。上一届政府之后,采集尾静脉血检测血清骨保护素(OPG)浓度,碱性磷酸酶（ALP）和骨钙蛋白（BPG）。H-E染色观察上颌骨缺损区的病理变化,并进行了LaneSandhu评分。应用抗酒石酸酸性磷酸酶(TRAP)染色检测缺损区的破骨细胞数目。实时荧光定量PCR(RT-qPCR)和Westernblot(WB)检测Wnt,β-catenin和Runx2mRNA蛋白表达。采用SPSS23.0软件包进行统计学分析。
结果：与N组相比，OPG的浓度,ALP,M组BGP和LaneSandhu评分下降，破骨细胞数量增加。与M组相比,OPG的浓度,ATV组ALP、BGP和LaneSandhu评分增加，破骨细胞数量减少。H-E染色后,N组上颌骨缺损区骨形成量较多，M组缺损区骨组织较少，ATV组缺损区骨组织数量增加。与N组相比,Wnt,β-catenin和Runx2mRNA蛋白降低。与M组相比,Wnt,β-catenin和Runx2mRNA蛋白表达增加。
结论：阿托伐他汀可促进大鼠牙槽骨缺损愈合，加速骨重建。这种效应可能与Wnt/β-catenin信号通路的激活有关。
方法:30只大鼠随机分为正常组(N组),模型组(M组)和阿托伐他汀给药组(ATV组)。除N组外,在其他大鼠牙槽骨中制作骨缺损，以构建牙槽骨缺损模型。建模成功后,ATV组20mg/kg阿托伐他汀混悬液灌胃给药,N组和M组灌胃给予等量的羧甲基纤维素钠溶液21天。上一届政府之后,采集尾静脉血检测血清骨保护素(OPG)浓度,碱性磷酸酶（ALP）和骨钙蛋白（BPG）。H-E染色观察上颌骨缺损区的病理变化,并进行了LaneSandhu评分。应用抗酒石酸酸性磷酸酶(TRAP)染色检测缺损区的破骨细胞数目。实时荧光定量PCR(RT-qPCR)和Westernblot(WB)检测Wnt,β-catenin和Runx2mRNA蛋白表达。采用SPSS23.0软件包进行统计学分析。
结果：与N组相比，OPG的浓度,ALP,M组BGP和LaneSandhu评分下降，破骨细胞数量增加。与M组相比,OPG的浓度,ATV组ALP、BGP和LaneSandhu评分增加，破骨细胞数量减少。H-E染色后,N组上颌骨缺损区骨形成量较多，M组缺损区骨组织较少，ATV组缺损区骨组织数量增加。与N组相比,Wnt,β-catenin和Runx2mRNA蛋白降低。与M组相比,Wnt,β-catenin和Runx2mRNA蛋白表达增加。
结论：阿托伐他汀可促进大鼠牙槽骨缺损愈合，加速骨重建。这种效应可能与Wnt/β-catenin信号通路的激活有关。
