Objective To explore the effects of aspirin on formation and dispersion of Pseudomonas aeruginosa (P.aeruginosa) biofilm.Methods The broth microdilution method was used to detect the minimal inhibitory concentration(MIC) of aspirin for P.aeruginosa.The anti-biofilm effects of aspirin on P.aeruginosa were determined on the microtiter plates combined with crystal violet staining.The serial dilution method for counting colony number on microtiter plate was used to explore the effects of aspirin on initial adherence of P.aeruginosa.Results The MIC values of aspirin against PAO1,PA18,PA53 and PA67 strains of Pseudomonas aeruginosa were 5,2.5,5 and 5 mg/mL respectively.Aspirin significantly inhibited the formation and dispersion of the biofilm of PAO1 and PA18 strains (t =5.65,P ＜ 0.05 and t =5.06,P ＜ 0.05 for inhibition;t =6.45,P ＜ 0.05 and t =6.26,P ＜ 0.05 for dispersion) at the concentration of 2.5 mg/mL.Similar effects were also found in the determination for PA67 and PA53 strains(t =6.45,P ＜0.05 and t =6.26,P ＜ 0.05 for inhibition;t =7.82,P ＜ 0.05;t =9.18,P ＜ 0.05 for dispersion) at aspirin concentration of 1.25 and 0.313 mg/mL respectively.Aspirin inhibited the initial adherence of P.aeruginosa at the concentration of 2.5 mg/mL(P ＜0.05).Conclusion Aspirin could significantly inhibit the initial adherence and biofilm formation of P.aeruginosa and disperse the 24 hour-formed mature bioiflm.

AIM: With building a proliferation model of PA-induced VSMC, the effect of ATGL, a key fat metabolism enzyme, on the phenotype transformation of VSMC was preliminarily explored. METHODS: 40 μmol/L Atglistatin was added to the proliferation model of VSMC induced by PA (50 μmol/L, 100 μmol/L, and 200 μmol/L, respectively) at separately administered concentrations, and cell viability and cell proliferation were detected by CCK-8 and EDU; cell migration ability was detected by scratch assay; oil red staining was used to detect the accumulation of lipid droplets in VSMC was detected by oil red staining; the effects of PA on ATGL as well as the effects of smooth muscle contraction phenotype proteins were examined by Western blot. RESULTS: PA at a concentration of 100 μmol/L could significantly induce VSMC proliferation, promote lipophagy and increase lipid droplet accumulation in VSMC; meanwhile, Atglistatin could exacerbate these changes caused by PA and increase lipid droplet accumulation in VSMC. CONCLUSION: Atglistatin exacerbates PA-induced VSMC proliferation and increases VSMC lipid droplet accumulation, and exacerbates transformation of proliferative phenotype of VSMC.