牙龈卟啉单胞菌
炎症
信号转导
癌症研究
肝细胞
脂肪肝
牙周炎
NF-κB
发病机制
牙周病原体
生物
免疫学
医学
体外
细胞生物学
病理
内科学
疾病
生物化学
作者
Chao Yao,Dongmei Lan,Xue Li,Yan Wang,Shengcai Qi
摘要
Abstract Objective Non‐alcoholic fatty liver disease (NAFLD) is a clinicopathological syndrome characterized by excessive fat deposition in hepatocytes caused by non‐alcoholic liver injury. Porphyromonas gingivalis ( P.g ) is the main pathogen causing periodontitis, which can aggravate the progression of NAFLD in our previously study. The objective of this study was to further investigate the pathogenesis and moleculer michanisma of NAFLD aggravated by P.g . Methods A mouse model of NAFLD was established, and the changes of inflammatory factors and NF‐κB signaling pathway in liver tissue and L‐02 cells were analyzed by transcriptome sequencing, Western blot, IHC and RT‐PCR. In addition, the NF‐κB signaling pathway inhibitor QNZ and ferroptosis inhibitor Fer‐1 were used to analyze the relationship between NF‐κB signaling pathway and ferroptosis in vitro. Results In vivo and in vitro experiments, P.g can induce liver inflammation and activate NF‐κB signaling pathway. At the same time, P.g promotes ferroptosis and inflammation in L‐02 in vitro. QNZ alleviates ferroptosis and inflammatory activation in L‐02. Fer‐1 can relieve the L‐02 inflammation caused by P.g products . Conclusion Porphyromonas gingivalis can induce ferroptosis and inflammation in hepatocytes and further worsen liver lesions. The mechanism of ferroptosis in hepatocytes depends on NF‐κB signaling pathway, which provides a new strategy for clinical treatment and prevention of NAFLD.
科研通智能强力驱动
Strongly Powered by AbleSci AI