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格列本脲抑制创伤性咬合诱导的大鼠骨吸收。

Glyburide inhibits the bone resorption induced by traumatic occlusion in rats.

机构信息

Section of Periodontology, Department of Odontology, Fukuoka Dental College, Fukuoka, Japan.

Oral Medicine Research Center, Fukuoka Dental College, Fukuoka, Japan.

出版信息

J Periodontal Res. 2020 Jun;55(3):464-471. doi: 10.1111/jre.12731. Epub 2020 Mar 10.

Abstract

OBJECTIVE

To examine whether glyburide inhibits bone destruction caused by traumatic occlusion in a rat occlusal trauma model.

BACKGROUND

Excessive mechanical stress, such as traumatic occlusion, induces expression of IL-1β and may be involved in bone resorption. NLRP3 inflammasomes have been linked to IL-1β expression, but it is currently unclear whether glyburide, the inhibiter of NLRP3 inflammasome, suppresses occlusal trauma in rats.

METHODS

Male SD rats aged 7 weeks were used. In the trauma group, the occlusal surface of the maxillary first right molar was raised by attaching a metal wire to apply occlusal trauma to the mandibular first right molar. In the trauma + glyburide group, the NLRP3 inhibitor glyburide was administered orally every 24 hours from 1 day before induction of occlusal trauma. Rats were euthanized after 5 or 10 days, and the maxillary first molars were harvested with the adjacent tissues for histopathological investigation. Immunohistochemical expression of IL-1β, NLRP3, and RANKL was also assessed.

RESULTS

On day 5, bone resorption was significantly greater in the trauma group compared with the control group or the trauma + glyburide group, and there were significantly higher numbers of osteoclasts and cells positive for IL-1β, NLRP3, and RANKL in the trauma group.

CONCLUSION

In this study, glyburide inhibits bone resorption by traumatic occlusion in rats. It suggests that the NLRP3/IL-1β pathway might be associated with bone resorption induced by traumatic occlusion.

摘要

目的

研究格列本脲是否能抑制创伤性咬合大鼠咬合创伤模型中的骨破坏。

背景

过度的机械应力,如创伤性咬合,会诱导白细胞介素-1β(IL-1β)的表达,并可能参与骨吸收。NLRP3 炎性小体与 IL-1β 的表达有关,但目前尚不清楚作为 NLRP3 炎性小体抑制剂的格列本脲是否能抑制大鼠的咬合创伤。

方法

选用 7 周龄雄性 SD 大鼠。在创伤组中,通过在上颌第一右侧磨牙的咬合面上附加金属丝,施加咬合创伤于下颌第一右侧磨牙。在创伤+格列本脲组中,从诱导咬合创伤前 1 天开始,每天 24 小时口服给予 NLRP3 抑制剂格列本脲。在 5 天或 10 天后处死大鼠,取上颌第一磨牙及其邻近组织进行组织病理学研究。还评估了 IL-1β、NLRP3 和 RANKL 的免疫组织化学表达。

结果

第 5 天,与对照组或创伤+格列本脲组相比,创伤组的骨吸收明显增加,且创伤组的破骨细胞数量和 IL-1β、NLRP3 和 RANKL 阳性细胞数量明显增加。

结论

本研究表明,格列本脲抑制了大鼠因创伤性咬合导致的骨吸收。这提示 NLRP3/IL-1β 通路可能与创伤性咬合诱导的骨吸收有关。

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