Abstract: Objective To observe the protective effect of lidocaine on cysteinyl aspartate specific proteinase-1(caspase-1) and interleukin-1β (IL-1β) in lipopolysaccharide-induced inflammation in mice and to investigate its mechanism. Methods Monolayer cultured mouse macrophages in six-well plates were randomly divided into 4 groups:control group, lidocaine group, lipopolysaccharide group, and lidocaine+lipopolysaccharide group. Cell apoptosis rate was measured with flow cytometry. Expressions of caspase-1 and IL-1β mRNA were detected with realtime PCR (RT-PCR). The protein concentrations of caspase-1 and IL-1β in the culture medium were assessed with enzyme-linked immunosorbent assay (ELISA). Results Compared with control group, in lidocaine group, the apoptosis rate, mRNA expression and protein expression of caspase-1 and IL-1β had no significant change (P>0.05); in the lipopolysaccharide group, the apoptosis rate, mRNA expression and protein expression of caspase-1 and IL-1β were significantly higher (all P<0.05). Compared with the lipopolysaccharide group, in lidocaine+lipopolysaccharide group, apoptosis was significantly reduced (P<0.05), mRNA and protein expression levels of caspase-1 and IL-1β expressions were markedly lower (P<0.05). Conclusion Lidocaine can reduce apoptosis in murine macrophages lipopolysaccharide-induced inflammatory response. Protective effects of lidocaine on tissue inflammation may be related to inhibition ofcaspase-1 and IL-1β.

Key words: Lidocaine, Lipopolysaccharides, Cysteinyl aspartate specific proteinase-1, Interleukin-1β, Inflammation, Apoptosis