Archives of oral biology · 2021
Targeting the Nod-like receptor protein 3 Inflammasome with inhibitor MCC950 rescues lipopolysaccharide-induced inhibition of osteogenesis in Human periodontal ligament cells.
СтатьяНазвание и аннотация: Перевод в очереди
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Peng Wei, Zhang Bo, Sun Zhengfan, Zhang Meifeng, Guo Ling
Аннотация
OBJECTIVE: We aim to investigate whether lipopolysaccharide-stimulated activition of Nod-like receptor protein 3 (NLRP3) Inflammasome inhibits osteogenesis in Human periodontal ligament cells (HPDLCs). Futhermore, to study whether MCC950 (a inhibitor of NLRP3 Inflammasome) rescues lipopolysaccharide-induced inhibition of osteogenesis in HPDLCs as well as the underlying mechanisms.
METHODS: HPDLCs were isolated from periodontal ligament of healthy orthodontic teeth from teenagers, and cells surface marker protein were detected by flow cytometry. Cells viability were determined by Cell Counting kit 8 assay. Enzyme-linked immunosorbent assay was used to analyze the secretion of proinflammatory factors. Western blot and real-time quantitative polymerase chain reaction (RT-qPCR) were measured assessing the expression of NLRP3 and Caspase-1. RT-qPCR, Alizarin red staining and Alkaline phosphatase staining were tested to determine the osteogenic differentiation capacity of HPDLCs.
RESULTS: It was found that lipopolysaccharide in the range of concentrations from 10 to 100 μg/ml significantly inhibited HPDLCs viability at 24 h and significantly improved proinflammatory cytokine expressions at 8 h and 24 h. MCC950 reversed lipopolysaccharide-stimulated proinflammatory cytokine expressions including interleukin-1β and interleukin-18, but not tumor necrosis factor-α. In addition, MCC950 rescued the lipopolysaccharide-inhibited osteogenic gene (Alkaline phosphatase, Runt-related transcription factor 2, and Osteocalcin). Moreover, MCC950 downregulated lipopolysaccharide-induced relative protein of NLRP3 Inflammasome signaling pathway, such as NLRP3 and Caspase-1.
CONCLUSION: MCC950 rescues lipopolysaccharide-induced inhibition of osteogenesis in HPDLCs via blocking NLRP3 Inflammasome signaling pathway, and it may be used as a promising therapeutic agent for periodontitis or periondontal regenerative related disease.
METHODS: HPDLCs were isolated from periodontal ligament of healthy orthodontic teeth from teenagers, and cells surface marker protein were detected by flow cytometry. Cells viability were determined by Cell Counting kit 8 assay. Enzyme-linked immunosorbent assay was used to analyze the secretion of proinflammatory factors. Western blot and real-time quantitative polymerase chain reaction (RT-qPCR) were measured assessing the expression of NLRP3 and Caspase-1. RT-qPCR, Alizarin red staining and Alkaline phosphatase staining were tested to determine the osteogenic differentiation capacity of HPDLCs.
RESULTS: It was found that lipopolysaccharide in the range of concentrations from 10 to 100 μg/ml significantly inhibited HPDLCs viability at 24 h and significantly improved proinflammatory cytokine expressions at 8 h and 24 h. MCC950 reversed lipopolysaccharide-stimulated proinflammatory cytokine expressions including interleukin-1β and interleukin-18, but not tumor necrosis factor-α. In addition, MCC950 rescued the lipopolysaccharide-inhibited osteogenic gene (Alkaline phosphatase, Runt-related transcription factor 2, and Osteocalcin). Moreover, MCC950 downregulated lipopolysaccharide-induced relative protein of NLRP3 Inflammasome signaling pathway, such as NLRP3 and Caspase-1.
CONCLUSION: MCC950 rescues lipopolysaccharide-induced inhibition of osteogenesis in HPDLCs via blocking NLRP3 Inflammasome signaling pathway, and it may be used as a promising therapeutic agent for periodontitis or periondontal regenerative related disease.