Introduction Preeclampsia (PE) is a clinical complication of pregnancy associated with elevated serum levels of inflammatory cytokines, leukocyte activation and oxidative stress. Autophagy is an intracellular catabolic process responsible for the cellular homeostasis maintenance. This process has a potent anti-inflammatory mechanism that controls the inflammasomes, which can be activated by monosodium urate (MSU) and hyaluronan (HA), resulting in release of active forms of Interleukin-1 beta (IL-1 β ) and IL-18. Objectives This study investigated the autophagy-related gene expression in monocytes from pregnant women with PE stimulated or not with MSU and HA. Methods Monocytes were obtained from peripheral blood of 20 preeclamptic (PE) pregnant women and 20 normotensive (NT) pregnant women and cultured in the presence or absence of 50 μ g/mL of MSU or 100 μ g/mL of HA for 4h. Additionally, monocytes from 20 healthy non-pregnant (NP) women were incubated with 20 and 40pg/mL of IL-1 β and TNF- α for 4h. Autophagy activation was evaluated by mRNA for Beclin-1, LC3-II and p62 by RT-qPCR in unstimulated monocytes or after cell stimulation with MSU or HA. The results were analyzed using non-parametric tests at 5% significance level. Results It was observed a higher gene expression of Beclin-1, LC3-II and p62 in monocytes from PE group cultured in the absence of MSU and HA when compared to NT group. In preeclamptic group, MSU and HA induced higher expression of mRNA for Beclin-1, LC3-II and p62 compared to endogenous levels. Furthermore, after MSU stimulation, monocytes from NT group expressed higher LC3-II and p62 mRNA levels when compared to endogenous NT group. In monocytes from non-pregnant women, IL-1 β and TNF- α , at concentrations of 20 and 40pg/mL induced higher gene expression of p62 in a dose-dependent manner compared to unstimulated cells. Conclusion The basal up-regulation of Beclin-1, LC3-II and p62 mRNA expression in monocytes from preeclamptic women confirms the autophagy activation in these cells. Stimuli with MSU and HA increased the gene expression of autophagy in monocytes from pregnant women with PE, suggesting that these DAMPs may contribute to the inflammasome activation and, consequently, enhancing the autophagy activity, in order to control this inflammatory complex involved in the PE pathogenesis.