Abstract: Objective In this study, NK-1 receptor antagonist was given to block the function of substance P (SP) in periodontitis model mice and cell experiments in vitro to explore the role of SP in multi-organ dysfunction induced by systemic inflammatory response caused by periodontitis. Methods Periodontitis mouse model was induced by repeated gingival sulcus injection of Porphyromonas gingivalis lipopolysaccharides (LPS). At the same time, NK-1 receptor antagonist was given to observe the secretion of systemic inflammatory factors and functional damage of various organs in periodontitis mice; macrophages were stimulated by LPS and SP respectively, and IL-1β in the supernatant was monitored by enzyme-linked immunosorbent assay(ELISA); NK-1 receptor antagonist was added to observe the IL-1β level in supernatant. Results Compared with the control group, SP in gingival crevicular fluid and serum in LPS induced periodontitis group were significantly increased (P<0.001), and the level of IL-1β, IL-6 and TNF- α in serum was also significantly increased (P<0.001). Alanine aminotransferase(ALT) and aspartate aminotransferase (AST) increased slightly in LPS group (P<0.05), and there was significant difference in lung histopathological score (P<0.001). NK-1 receptor antagonist decreased IL-1β in serum, and the level of ALT was significantly lower than that in LPS group (P<0.05). NK-1 receptor antagonist could partially reverse the production of IL-1β secreted by macrophages induced by SP(P<0.001). Conclusion SP participates in the appearance of multi-organ dysfunction induced by systemic inflammatory response caused by periodontitis through binding with NK-1 receptor.

Key words: lipopolysaccharide, periodontitis, substance P, inflammatory factor, multi-organ dysfunction