坏死性下垂
牙周炎
牙龈卟啉单胞菌
污渍
肿瘤坏死因子α
破骨细胞
HMGB1
化学
程序性细胞死亡
细胞生物学
炎症
生物
细胞凋亡
免疫学
医学
体外
生物化学
内科学
基因
作者
Liangyu Tan,Wei-Cheng Chan,Jing Zhang,Jiajia Wang,Zizheng Wang,Jie Liu,Jiaxin Li,Xinran Liu,Min Wang,Liang Hao,Yuan Yue
摘要
Abstract Objective To explore the mechanism of receptor‐interacting protein 1 (RIP1)‐mediated necroptosis during periodontitis progression. Background RIP3 and mixed lineage kinase domain‐like protein (MLKL) have been detected to be upregulated in periodontitis models. Because RIP1 is involved in necroptosis, it might also play a role in the progression of periodontitis. Methods An experimental periodontitis model in BALB/c mice was established by inducing oral bacterial infection. Western blotting and immunofluorescence analyses were used to detect RIP1 expression in the periodontal ligament. Porphyromonas gingivalis was used to stimulate L929 and MC3T3‐E1. RIP1 was inhibited using small‐interfering RNA. Western blotting, reverse transcription‐quantitative polymerase chain reaction (RT‐qPCR), and enzyme‐linked immunosorbent assay (ELISA) analyses were used to detect the effect of necroptosis inhibition on the expression of damage‐associated molecular patterns and inflammatory cytokines. Necrostatin‐1 (Nec‐1) was intraperitoneally injected to inhibit RIP1 expression in mice. Necroptosis activation and inflammatory cytokine expression in periodontal tissue were verified. Tartrate‐resistant acid phosphatase staining was applied to observe osteoclasts in the bone tissues of different groups. Results RIP1‐mediated necroptosis was activated in mice with periodontitis . P. gingivalis induced RIP1‐mediated necroptosis in L929 and MC3T3‐E1 cells. After RIP1 inhibition, the expression levels of high mobility group protein B1 (HMGB1) and inflammatory cytokines were downregulated. After inhibiting RIP1 with Nec‐1 in vivo, necroptosis was also inhibited, the expression levels of HMGB1 and inflammatory cytokines were downregulated, and osteoclast counts in the periodontal tissue decreased. Conclusion RIP1‐mediated necroptosis plays a role in the pathological process of periodontitis in mice. Nec‐1 inhibited necroptosis, alleviated inflammation in periodontal tissue, and reduced bone resorption in periodontitis.
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