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N-苯甲酰甲基溴化噻唑鎓抑制晚期糖基化终产物(AGE)-AGE受体轴,以调节大鼠实验性牙周炎。

N-Phenacylthiazolium bromide inhibits the advanced glycation end product (AGE)-AGE receptor axis to modulate experimental periodontitis in rats.

作者信息

Chang Po-Chun, Tsai Sheng-Chueh, Chong Li Yen, Kao Man-Jung

机构信息

Graduate Institute of Clinical Dentistry, School of Dentistry, National Taiwan University, Taipei, Taiwan.

出版信息

J Periodontol. 2014 Jul;85(7):e268-76. doi: 10.1902/jop.2014.130554. Epub 2014 Feb 7.

DOI:10.1902/jop.2014.130554
PMID:24988129
Abstract

BACKGROUND

Advanced glycation end products (AGEs) are involved in the inflammatory process and are considered to be etiologic factors of diabetic periodontitis. The purpose of this study is to investigate the capability of N-phenacylthiazolium bromide (PTB), a glycated cross-link breaker, in the modulation of periodontitis in various disease phases.

METHODS

Mitogenesis and cytotoxicity of human periodontal ligament cells (hPDLCs) undergoing PTB treatment were evaluated in vitro. In vivo biomodulation was investigated by systemically administering PTB in the induction, progression, and recovery phases of ligature-induced periodontitis in rats, with the results evaluated by microcomputed tomography, histology, immunohistochemistry of the AGE and AGE receptor (RAGE), and gene expression of tumor necrosis factor-α (TNF-α), RAGE, periostin, fibronectin, and type I collagen.

RESULTS

Significantly promoted mitogenesis and reduced cytotoxicity of hPDLCs were noted with 0.05 to 0.1 mM PTB treatment at 24 hours. Systemic PTB administration significantly reduced periodontal bone loss, AGE deposition, and expressions of TNF-α and RAGE but elevated the periostin level in all three phases of periodontitis.

CONCLUSION

PTB inhibits the induction and progression of periodontitis and facilitates its recovery via improving cellular viability and inhibiting the AGE-RAGE axis.

摘要

背景

晚期糖基化终末产物(AGEs)参与炎症过程,被认为是糖尿病性牙周炎的病因。本研究旨在探讨糖化交联破坏剂N-苯甲酰噻唑溴化物(PTB)在不同疾病阶段对牙周炎的调节能力。

方法

体外评估接受PTB处理的人牙周膜细胞(hPDLCs)的促有丝分裂作用和细胞毒性。通过在大鼠结扎诱导性牙周炎的诱导、进展和恢复阶段全身给予PTB来研究体内生物调节作用,结果通过微型计算机断层扫描、组织学、AGE和AGE受体(RAGE)的免疫组织化学以及肿瘤坏死因子-α(TNF-α)、RAGE、骨膜蛋白、纤连蛋白和I型胶原的基因表达进行评估。

结果

在24小时时,0.05至0.1 mM PTB处理显著促进了hPDLCs的促有丝分裂作用并降低了细胞毒性。全身给予PTB在牙周炎的所有三个阶段均显著减少了牙周骨丢失、AGE沉积以及TNF-α和RAGE的表达,但提高了骨膜蛋白水平。

结论

PTB通过改善细胞活力和抑制AGE-RAGE轴来抑制牙周炎的诱导和进展,并促进其恢复。

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N-Phenacylthiazolium bromide inhibits the advanced glycation end product (AGE)-AGE receptor axis to modulate experimental periodontitis in rats.N-苯甲酰甲基溴化噻唑鎓抑制晚期糖基化终产物(AGE)-AGE受体轴,以调节大鼠实验性牙周炎。
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