Figure 3.

Gestational complications reflect the continuity of placental dysfunction, and n-3 PUFAs may improve pregnancy outcomes through their anti-inflammatory and antioxidant effects. The primary mechanisms of the anti-inflammatory action of n-3 PUFAs include: A) N-3 PUFAs produce SPMs via the LOX and COX pathways ⁵³; B) N-3 PUFAs inhibit the phosphorylation of the inhibitory subunit IκB of NFκB, leading to reduced activation of the pro-inflammatory transcription factor NFκB. N-3 PUFAs also compete with lipopolysaccharides (LPS) and saturated fatty acids (SFA) to bind and activate toll-like receptors, such as TLR-4, inhibiting the activation of NF-κB ¹⁹⁹; C) N-3 PUFAs suppress the activation of the NLRP3 inflammasome through GPR40 and GPR120-dependent pathways ⁵². Research on the anti-oxidant mechanisms of n-3 PUFAs is relatively limited, but can currently be summarized as follows ¹⁹¹, ¹⁹², ²⁰⁰: D) N-3 PUFAs can improve the status of peroxidases, such as increasing the activity of superoxide dismutase (SOD) and glutathione peroxidase (GSH-Px); E) N-3 PUFAs can lower levels of phagocyte and tissue-specific NADPH oxidases (NOX), which are significant contributors to ROS production. N-3 PUFAs may also inhibit NOX generation by competing to reduce the synthesis of AA, a primary activator of NOX; F) DHA can enhance the expression of antioxidant-related genes (such as SIRT1 and BRCA1/MSH2), which are crucial for DNA repair.