S1P1在根尖周病发病机制中的作用
首发时间:2017-05-17
摘要:目的:观察大鼠根尖周病发展过程中S1P1的表达及变化,并分析其与 RANKL的表达以及破骨细胞的数量之间的关系,以探讨S1P1以及S1P1-RANKL信号轴参与根尖周病病理过程的作用及机制。方法:将实验一中制备的各时期根尖周组织切片通过免疫组织化学染色法检测并分析 S1P1和RANKL的表达与变化,通过TRAP染色法检测和分析破骨细胞的表达与变化,并统计分析S1P1与RANKL/TRAP表达的相关性。结果:开髓7天后可检测到S1P1阳性的细胞表达于根尖周病损,S1P1的表达在炎症急性期(开髓后14天至21天)达到高峰;当炎症进入慢性期(开髓后28天至35天),S1P1的表达逐渐降低并趋于稳定。RANKL及破骨细胞(即TRAP阳性细胞)的表达亦表现出同样趋势。相关性分析提示S1P1与RANKL/破骨细胞的表达均呈正相关。根尖周病损中存在S1P1和RANKL共表达的细胞,该细胞在急性期表达较强,慢性期则较弱。结论:S1P1在根尖周病的病变发展过程中,上调RANKL表达,从而上调破骨细胞的分化及功能,从而导致根尖周骨缺损的形成。 S1P1及其相关信号轴(S1P1-RANKL)在根尖周病损的形成和炎症进展的过程中起着重要作用。
关键词: 骨破坏;破骨细胞;RANKL;S1P1
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Dissecting the role of S1P1 in apical periodontitis
Abstract:Objective: The purpose of the present study was to investigate the expression of S1P1 in rat periapical lesions and its relationship with receptor activator of nuclear factor kappa B ligand (RANKL) and osteoclasts. Methods: Periapical lesions were induced and rats were sacrificed on day 0, 7, 14, 21, 28, and 35, and their mandibles were harvested (experiment 1) for immunohistochemistry, enzyme histochemistry, and double immunofluorescence analysis. Results: S1P1-positive cells were observed in the inflammatory periapical regions; the number of S1P1-positive cells peakDissecting the role of Sphingosine 1-Phosphate receptor 1 in apical periodontitised at day 14, and then decreased from day 21 to day 35. The distribution of S1P1-positive cells was positively correlated with the dynamics of RANKL-positive cells and osteoclasts. S1P1 and RANKL double-positive cells were found in the acute (higher) and chronic (lower) phases of periapical lesions. Conclusions: S1P1 expression was confirmed in rat periapical lesions; it was positively correlated with RANKL and osteoclasts expression and is therefore a contributing factor to the pathogenesis of periapical lesions.
Keywords: Bone resorption osteoclast RANKL S1P1
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