18*-glycyrrhetinic acid inhibits periodontitis via glucocorticoid-independent nuclear factor-*B inactivation in interleukin-10-deficient mice.
18*-glycyrrhetinic acid inhibits periodontitis via glucocorticoid-independent nuclear factor-*B inactivation in interleukin-10-deficient mice.
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18*-甘草次酸通过白细胞介素 10 缺陷小鼠体内不依赖糖皮质激素的核因子 -*B 失活来抑制牙周炎。
DOI：
10.1111/j.1600-0765.2010.01296.x
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发表时间：
2010
影响因子：
3.5
通讯作者：
Stashenko,P
中科院分区：
文献类型：
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作者：
Sasaki,H;Suzuki,N;Alshwaimi,E;Xu,Y;Battaglino,R;Morse,L;Stashenko,P
陈志刚，陈志刚，陈志刚，陈志刚，陈志刚。18β -甘草次酸对小鼠牙周炎的抑制作用。journal of chengdu electromechanical college; 2010；45: 757 - 763。©2010 John Wiley & Sons A/ s背景和目的：18β‐Glycyrrhetinic acid （GA）是从甘草根提取物（Glycyrrhiza glabra）中提取的天然抗炎化合物。本研究探讨了GA对实验性牙周炎的影响及其作用机制。材料与方法：采用白细胞介素- 10 -缺乏小鼠口腔感染牙龈卟啉单胞菌w83诱导牙周炎。在首次感染后的第42天，研究人员检测了GA对牙槽骨丢失和牙龈基因表达的影响，GA在预防或治疗方案中通过皮下注射给予。GA对脂多糖（LPS）刺激的巨噬细胞、T细胞增殖和破骨细胞生成的影响也在体外进行了研究。结果：无论是预防还是治疗，18β -甘草次酸都能显著减少感染引起的白介素- 10缺失小鼠的骨质流失，这些小鼠是高度易感的疾病。虽然有报道称GA通过下调11β -羟基类固醇脱氢酶- 2 （HSD2）发挥其抗炎活性，HSD2可将活性糖皮质激素转化为非活性形式，但GA并没有降低牙龈组织中ehsd2基因的表达。相反，在无糖皮质激素的条件下，GA有效地抑制LPS刺激的促炎细胞因子产生和RANKL刺激的破骨细胞生成，这两者都依赖于核因子κB。此外，GA在体外抑制LPS -和RANKL -刺激的核因子κB p105磷酸化。结论：这些发现表明，GA通过使核因子κB失活，以一种不依赖于白细胞介素- 10和糖皮质激素的方式抑制牙周炎。
Sasaki H, Suzuki N, AlShwaimi E, Xu Y, Battaglino R, Morse L, Stashenko P. 18β‐Glycyrrhetinic acid inhibits periodontitis via glucocorticoid‐independent nuclear factor‐κB inactivation in interleukin‐10‐deficient mice. J Periodont Res 2010; 45: 757–763. © 2010 John Wiley & Sons A/SBackground and Objective:18β‐Glycyrrhetinic acid (GA) is a natural anti‐inflammatory compound derived from licorice root extract (Glycyrrhiza glabra). The effect of GA on experimental periodontitis and its mechanism of action were determined in the present study.Material and Methods:Periodontitis was induced by oral infection withPorphyromonas gingivalisW83 in interleukin‐10‐deficient mice. The effect of GA, which was delivered by subcutaneous injections in either prophylactic or therapeutic regimens, on alveolar bone loss and gingival gene expressions was determined on day 42 after initial infection. The effect of GA on lipopolysaccharide (LPS)‐stimulated macrophages, T cell proliferation and osteoclastogenesis was also examinedin vitro.Results:18β‐Glycyrrhetinic acid administered either prophylactically or therapeutically resulted in a dramatic reduction of infection‐induced bone loss in interleukin‐10‐deficient mice, which are highly disease susceptible. Although GA has been reported to exert its anti‐inflammatory activity via downregulation of 11β‐hydroxysteroid dehydrogenase‐2 (HSD2), which converts active glucocorticoids to their inactive forms, GA did not reduceHSD2gene expression in gingival tissue. Rather, in glucocorticoid‐free conditions, GA potently inhibited LPS‐stimulated proinflammatory cytokine production and RANKL‐stimulated osteoclastogenesis, both of which are dependent on nuclear factor‐κB. Furthermore, GA suppressed LPS‐ and RANKL‐stimulated phosphorylation of nuclear factor‐κB p105in vitro.Conclusion:These findings indicate that GA inhibits periodontitis by inactivation of nuclear factor‐κB in an interleukin‐10‐ and glucocorticoid‐independent fashion.