Background Evidence that a vegetarian diet rich in antioxidants contributes to cardiovascular health are growing, however, the underlying molecular mechanisms remain unknown. HO‐1 (heme‐oxygenase‐1), a marker of adaptive response, is protective against oxidative stress and has shown cardioprotective effects. Therefore, we evaluated circulating HO ‐1 levels and the effect of plasma from omnivorous and vegetarians in endothelial cells (human umbilical vein endothelial cells) on modulating NRF2 (nuclear factor erythroid 2‐like 2)/HO ‐1 and nitric oxide production. Methods and Results From 745 participants initially recruited, 44 omnivorous and 44 vegetarian men matched by age and absence of cardiovascular risk factors and diseases were included in this study. Circulating HO ‐1 was measured using ELISA and human umbilical vein endothelial cells were incubated with plasma from omnivorous and vegetarians. Higher circulating HO ‐1 concentrations were found in omnivorous compared with vegetarians. Plasma from omnivorous and not from vegetarians induced NRF 2/ HO ‐1 and nitric oxide production in human umbilical vein endothelial cells, and increased reactive oxygen species production and caspase activity after incubation with stressor stimulus. Conclusions We suggest that HO ‐1 induction in omnivorous may indicate a pro‐oxidative status since HO ‐1 is activated under oxidative stress a state not seen in vegetarians.

Preeclampsia (PE) is a pregnancy-specific disorder that affects 3–8% expecting mothers worldwide being one of the main causes of maternal and fetal morbidity and mortality. The search for altered circulating molecules in PE is an important target to better understand the pathophysiology of this disease. Therefore, we evaluated Sirtuin-1 (SIRT1) concentration in plasma from healthy pregnant (HP) women, gestational hypertensive women (GH), and preeclampsia women (PE) via enzyme-linked immunosorbent assay (ELISA). We also measured intracellular SIRT1 in HUVECs incubated with plasma from PE patients compared to HP and GH via Western Blot Assay. Statistical differences were considered when p<0.05. SIRT1 was downregulated in PE compared to HP and GH, both in plasma and in in vitro assay. Similarly, SIRT1 was also reduced in pregnant women who subsequently developed PE (case) compared to women who had healthy pregnancies (control). This reduction may be indicative of possible underlying pathophysiology mechanisms in PE.

Preeclampsia (PE) is a specific syndrome of human pregnancy, being one of the main causes of maternal death. Persistent inflammation in the endothelium stimulates the secretion of several inflammatory mediators, activating different signaling patterns. One of these mechanisms is related to NLRP3 activation, initiated by high levels of danger signals such as cholesterol, urate, and glucose, producing IL-1, IL-18, and cell death by pyroptosis. Furthermore, reactive oxygen species (ROS), act as an intermediate to activate NLRP3, contributing to subsequent inflammatory cascades and cell damage. Moreover, increased production of ROS may elevate nitric oxide (NO) catabolism and consequently decrease NO bioavailability. NO has many roles in immune responses, including the regulation of signaling cascades. At the site of inflammation, vascular endothelium is crucial in the regulation of systemic inflammation with important implications for homeostasis. In this review, we present the important role of NLRP3 activation in exacerbating oxidative stress and endothelial dysfunction. Considering that the causes related to these processes and inflammation in PE remain a challenge for clinical practice, the use of drugs related to inhibition of the NLRP3 may be a good option for future solutions for this disease.

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