A peptide derived from rice inhibits alveolar bone resorption via suppression of inflammatory cytokine production
A peptide derived from rice inhibits alveolar bone resorption via suppression of inflammatory cytokine production
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DOI：
10.1002/wer.18-0630
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发表时间：
2019-10-01
影响因子：
4.3
通讯作者：
Yamazaki, Kazuhisa
中科院分区：
文献类型：
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作者：
Aoki-Nonaka, Yukari;Tabeta, Koichi;Yamazaki, Kazuhisa
背景牙周炎是一种炎症性疾病，由细菌抗原(如脂多糖)诱导产生炎性细胞因子，从而导致牙槽骨吸收。在此，我们评估了从大米中提取的淀粉-1-18肽在实验性牙周炎模型中的预防作用和对抗炎反应的影响。方法采用小鼠牙周炎模型，连续14d灌胃Amyl-1-18多肽，观察牙槽骨吸收、牙周组织促炎细胞因子基因转录及口腔内毒素水平。此外，将小鼠巨噬细胞与大肠杆菌或牙龈卟啉单胞菌的内毒素共同孵育，以分析Amyl-1-18对与促炎细胞因子产生相关的细胞信号通路的抑制作用，包括炎症体活性。结果口服amyl-1-18可抑制牙周炎模型大鼠牙槽骨吸收和IL-6基因转录，降低口腔内毒素水平，提示体内抑制内毒素活性对牙周炎有调节作用。此外，Amyl-1-18在体外可抑制脂多糖和重组IL-1β诱导的巨噬细胞产生IL-6，但对炎症体活性无影响。结论大米淀粉-1-18多肽通过抑制脂多糖诱导的炎症细胞因子的产生，抑制牙周炎模型小鼠牙槽骨的破坏。提示戊基-1-18肽具有抗炎作用，不仅通过中和内毒素，进而抑制核因子-kappaB信号转导，而且还通过抑制IL-1R相关信号转导途径发挥抗炎作用。
Background Periodontitis is an inflammatory disease that results in alveolar bone resorption due to inflammatory cytokine production induced by bacterial antigens such as lipopolysaccharides (LPS). Here, the preventive effect of the Amyl-1-18 peptide derived from rice in an experimental model of periodontitis and the effect on the anti-inflammatory response were assessed. Methods Alveolar bone resorption, gene transcription of proinflammatory cytokines in the gingiva, and the endotoxin level in the oral cavity were evaluated after oral administration of the Amyl-1-18 peptide for 14 days using a ligature-induced periodontitis model in mice. Additionally, murine macrophages were incubated with LPS of Escherichia coli or Porphyromonas gingivalis in the presence of Amyl-1-18 to analyze the suppressive effects of Amyl-1-18 on the cell signaling pathways associated with proinflammatory cytokine production, including inflammasome activities. Results Oral administration of Amyl-1-18 suppressed alveolar bone resorption and gene transcription of interleukin (il)6 in the gingiva of the periodontitis model, and decreased endotoxin levels in the oral cavity, suggesting modulation of periodontal inflammation by inhibition of endotoxin activities in vivo. Also, Amyl-1-18 suppressed IL-6 production induced by LPS and recombinant IL-1 beta in macrophages in vitro but had no effect on inflammasome activity. Conclusions The Amyl-1-18 peptide from rice inhibited alveolar bone destruction in mouse periodontitis model via suppressing inflammatory cytokine production induced by LPS. It was suggested that Amyl-1-18 peptide has anti-inflammatory property against LPS, not only by neutralization of LPS and subsequent inhibition of nuclear factor-kappa B signaling but also by inhibition of the IL-1R-related signaling cascade.