Abstract
Purpose: To investigate the protective effect of bisleuconothine A on periodontal tissue in rats and the mechanism involved.
 Methods: Adult male Sprague Dawley rats (n = 32) weighing 180 - 200 g (mean weight, 190 ± 10 g) were randomly assigned to four groups of eight rats each: control group, periodontitis group, bisleuconothine A (50 mg/kg) group and bisleuconothine A (100 mg/kg) group. Rats in the treatment groups received bisleuconothine intraperitoneally for two weeks. Periodontitis was induced in the rats using standard procedures. Serum and tissue samples were used for biochemical analysis. Alveolar bone loss was measured in rat maxillae, while the activity of bone alkaline phosphatase (BALP) was determined in serum. Tumor necrosis factor α (TNF-α) interleukin-1β and interleukin-6 (IL-1β and IL-6) were determined in gingival tissue using enzyme-linked immunosorbent assay (ELISA) kit. Gene and protein expressions of receptor activator of nuclear factor kappa-Β ligand (RANKL), osteoprotegerin (OPG), and matrix metallopeptidase-9 (MMP-9) were measured in gingival tissue using real-time quantitative polymerase chain reaction (qRT-PCR) and Western blotting, respectively.
 Results: Bisleuconothine A treatment significantly and dose-dependently reduced alveolar bone loss, as well as serum levels of TNF-α, IL-1β and IL-6, but increased BALP activity in periodontitis rats (p < 0.05). It also significantly and dose-dependently reduced mRNA expressions of RANKL and MMP-9, but significantly increased OPG mRNA expression (p < 0.05). Similarly, treatment with bisleuconothine A significantly and dose-dependently down-regulated RANKL, p-NF-kB, p-IkBα and iNOS proteins in gingival tissue of periodontitis rats (p < 0.05). The results of histopathological examination indicated that bisleuconothine A treatment significantly reversed histological changes in periodontal tissues of periodontitis rats. It also significantly reduced the degree of polymorphonuclear (PMN) cell infiltration in periodontal tissue.
 Conclusion: The results obtained show that bisleuconothine A protects periodontal tissue via the regulation of RANKL expression and infiltration of inflammatory cells.
 Keywords: Bisleuconothine A, Expression, Inflammation, Periodontitis, RANKL
Highlights
EXPERIMENTALPeriodontitis is a chronic inflammatory and infectious disease in which the integrity of gum tissue is disrupted [1]
Studies have shown that inflammatory cytokines such as IL-6 and IL-8 activate matrix metalloproteinases (MMPs), thereby promoting osteoclastogenesis [4]
This study investigated the protective effect of bisleuconothine A on periodontal tissue in rats and the mechanism involved
Summary
Periodontitis is a chronic inflammatory and infectious disease in which the integrity of gum tissue is disrupted [1]. Receptor activator of nuclear factor kappa-Β ligand (RANKL), known as tumor necrosis factor ligand superfamily member 11, tumor necrosis factor (TNF)-related activation-induced cytokine, OPG ligand or osteoclast differentiation factor, regulates cell proliferation by modifying Id4, Id2 and cyclin D1 protein levels. In humans, it is encoded by the TNFSF11 gene. This study investigated the protective effect of bisleuconothine A on periodontal tissue in rats and the mechanism involved. ImageJ image analysis software was used to determine the infiltration of inflammatory PMN cells into the gingival tissue of periodontitis rats.
Sign-in/Register to view highlights & summary Talk to us
Join us for a 30 min session where you can share your feedback and ask us any queries you have
Schedule a callDisclaimer: All third-party content on this website/platform is and will remain the property of their respective owners and is provided on "as is" basis without any warranties, express or implied. Use of third-party content does not indicate any affiliation, sponsorship with or endorsement by them. Any references to third-party content is to identify the corresponding services and shall be considered fair use under The CopyrightLaw.
