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

摘要

In this study, by constructing a rat model of orthodontic recurrence and intervening with coptisine, the IL-6, IL-8, TNF-a and soluble intercellular adhesion molecule-1 (sICAM-1) content were analyzed to assess the regulatory mechanism of copti-sine on the health status of recurrent periodontal tissue after orthodontics and the occurrence of periodontal tissue inflam-mation. 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 nor-mal 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 IP 203 8 109 20 On Tue, 05 Dec 2023 10:51:05 Genes and Genomes (KEGG) enrichment analysis, we found that Fas/FasL signaling pathway was enriched in pathways Copyright: American Scientific Publishers related to apoptosis, disease infection and inflammation. Western blot experiments confirmed that coptisine could inhibit Delivered by Ingenta Fas/FasL signaling activation in the process of relapse after orthodontics. Lipopolysaccharides (LPS) treatment signifi-cantly 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.

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