**Figure 3.** **Manipulating the autophagy affects NLRP3 inflammasomes.** (**A**) The immunoblot analysis of lysates of Mφ, which were left untreated or treated with rapamycin or 3-MA, and subsequently stimulated with ox-LDLs (50 ug/ml), or LPS and ATP for 24 hours. (**B**) The immunoblot analysis of lysates of Mφ, which were left untreated or treated with rapamycin or 3-MA, and subsequently stimulated with ox-LDLs (50 ug/ml), or LPS and ATP for 24 hours. (**A**–**C**) The densitometric analysis of the p62 signal and LC3II/LC3I ratio (**A**), the NLRP3, ASC, pro-caspase-1 and pro-IL-1β signal (**B**), and the p20 signal (**C**), which were normalized to β-actin. (**D**) The ELISA of IL-1β in the supernatants obtained from (**B**). (**E**) The immunoblot analysis of lysates of Mφ, which were left untreated or treated with rapamycin or bafilomycin A1, and subsequently stimulated with ox-LDLs (50 ug/ml) for 24 hours. The data are presented as mean ± SD (*n*=3); * denotes the statistical significance by one-way ANOVA with *post hoc* Dunnett’s multiple comparisons test. **P*<0.05, ***P*<0.01, ****P*<0.001.