Coptisine Down-Regulates Soluble Intercellular Adhesion Molecule-1 by Inactivating Fas/FasL Signaling Pathway to Inhibit the Recurrence After Orthodontics

In this study, by constructing a rat model of orthodontic recurrence and intervening with coptisine, the IL-6, IL-8, TNF-α and soluble intercellular adhesion molecule-1 (sICAM-1) content were analyzed to assess the regulatory mechanism of coptisine on the health status of recurrent periodontal tissue after orthodontics and the occurrence of periodontal tissue inflammation. Male rats were assigned into three groups by constructing coptisine liposome nano-objects: blank group (Blank, 10 rats), orthodontic tooth movement model group (50 rats). The orthodontic tooth movement model group was randomly divided into model group (module), model control group (control-free), model coptisine treatment group (treatment-free), model blank functional liposome group (control-lip) and model functional coptisine liposome group (treatment-lip). Rats in model group were killed on the day after device was removed. Rats in other groups received equal doses of normal saline, coptisine, blank functional liposomes, and functional coptisine liposomes by intragastric administration on the day of device removal and then were killed after 7 days of continuous treatment. Through Kyoto Encyclopedia of Genes and Genomes (KEGG) enrichment analysis, we found that Fas/FasL signaling pathway was enriched in pathways related to apoptosis, disease infection and inflammation. Western blot experiments confirmed that coptisine could inhibit Fas/FasL signaling activation in the process of relapse after orthodontics. Lipopolysaccharides (LPS) treatment significantly increased inflammatory cytokines and sICAM-1, as well as the level of Fas and FasL. Coptisine treatment inhibited LPS-induced Fas/FasL signaling pathway in periodontal ligament cells. Coptisine attenuated the relapsed inflammation after orthodontics by inhibiting Fas/FasL signaling.