Liu Fei, Huang Xin, He Jing-Jun, Song Ci, Peng Ling, Chen Ting, Wu Bu-Ling
International Medical Center, Guangdong Second Provincial General Hospital, Guangzhou, 510010, China; College of Stomatology, Southern Medical University, Guangzhou, 510515, China; Department of Stomatology, Nanfang Hospital, Guangzhou, 510515, China.
Department of Stomatology, Guangzhou Women and Children's Medical Center, Guangzhou Medical University, Guangzhou, 510515, China.
Microb Pathog. 2019 Feb;127:208-211. doi: 10.1016/j.micpath.2018.11.034. Epub 2018 Nov 23.
Periodontitis is an important inflammatory disease that often causes by periodontopathic bacteria. The present study, we tested the anti-inflammatory effects of plantamajoside on LPS-stimulated human gingival fibroblasts. Human gingival fibroblasts (HGFs) were stimulated with LPS from Porphyromonas gingivalis. Plantamajoside was administrated 1 h before LPS treatment. The results demonstrated that plantamajoside decreased the production of PGE, NO, IL-6, and IL-8 in LPS-stimulated HGFs. LPS-induced NF-κB p65 and IκB phosphorylation were also suppressed by plantamajoside. Furthermore, plantamajoside inhibited LPS-induced PI3K and AKT phosphorylation. In conclusion, these results suggested that the mechanism of plantamajoside was through inhibiting PI3K/AKT signaling pathway, which lead to the inhibition of NF-κB activation and inflammatory response.
牙周炎是一种重要的炎症性疾病，通常由牙周病原菌引起。在本研究中，我们测试了大车前苷对脂多糖（LPS）刺激的人牙龈成纤维细胞的抗炎作用。用人牙龈卟啉单胞菌的LPS刺激人牙龈成纤维细胞（HGFs）。在LPS处理前1小时给予大车前苷。结果表明，大车前苷降低了LPS刺激的HGFs中前列腺素E（PGE）、一氧化氮（NO）、白细胞介素-6（IL-6）和白细胞介素-8（IL-8）的产生。大车前苷还抑制了LPS诱导的核因子κB（NF-κB）p65和IκB的磷酸化。此外，大车前苷抑制了LPS诱导的磷脂酰肌醇-3激酶（PI3K）和蛋白激酶B（AKT）的磷酸化。总之，这些结果表明大车前苷的作用机制是通过抑制PI3K/AKT信号通路，从而导致NF-κB激活和炎症反应的抑制。
