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来自牙周炎的外体因子通过SCD-1/AMPK信号通路诱导肝硬化症

Chunmeng Ding¹, Zhenguo Shen¹, Ruonan Xu¹

¹College & Hospital of Stomatology, Anhui Medical University, Key Lab. of Oral Diseases Research of Anhui Province, Hefei 230032, China.

Biochimica et biophysica acta. Molecular basis of disease

|July 10, 2024

概括

牙周炎相关的外体细胞通过增加肝细胞中的脂肪合成来促进脂肪性肝病 (NAFLD). 这些外体对SCD-1进行上调并抑制AMPK通路,突出显示了口腔健康和肝脏脂肪代谢之间的联系.

科学领域:

口腔生物学口腔生物学
肝病学肝病学是一种肝病学.
细胞生物学细胞生物学

背景情况:

牙周炎与全身性疾病有关.
外基因组调解细胞间的通信.
肝细胞脂肪代谢对肝脏健康至关重要.

研究的目的:

研究牙周炎相关细胞外体在肝细胞脂肪代谢中的作用.
确定这些外体细胞通过哪些分子机制影响肝脏.
建立牙周炎和非酒精性脂肪性肝病 (NAFLD) 之间的联系.

主要方法:

用Porphyromonas gingivalis-lipopolysaccharide (Pg-LPS) 刺激巨细胞和人类牙周带纤维细胞 (hPDLFs).
用来自刺激细胞的外体对HepG2细胞进行治疗.
使用GW4869.9抑制外体释放.
在体内研究涉及对小鼠的尾静脉注射外体.
对基因表达 (SCD-1) 和信号通路 (AMPK) 的分析.

主要成果:

来自Pg-LPS刺激的巨细胞和hPDLFs的外基因组在HepG2细胞中诱导了脂生成.
牙周炎相关的外体在老鼠中促进了肝硬化和炎症.
在体内给药这些外体在小鼠中加剧了肝损伤和肥胖症.
外体细胞对SCD-1表达进行了上调,并抑制了肝细胞中的AMPK信号通路.

结论:

从牙周炎相关细胞中衍生出来的外体促进肝细胞脂肪生成.
这种促进通过SCD-1的上调和AMPK通路的抑制而发生.
研究结果支持监测口腔健康的重要性,以预防脂肪肝等口腔外疾病.

关键词:

外基因组是外基因组的组成部分.肝脏肥胖症肝脏肥胖症这是NAFLD.牙周病是指牙周病的发生.在 SCD-1/AMPK 信号通路上.

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