3.2.1. Lipoxin A4

LXA4 Inhibits the Progression of Endometrial Lesions in Experimental Studies

According to the studies evaluated here, treatment with LXA4 or the analog 15 epi-LXA4 performed according to the experimental model previously mentioned does not alter the mice's estrous cycle or ovarian function. Therefore, it does not prevent the development of endometriosis [27–29]. However, it inhibits established lesions' progression by significantly reducing endometriotic lesions' size and weight that histologically present a rudimentary architecture, with less glandular and stromal development [7,19,27–29,32,35].

LXA4 Attenuates Pro-Inflammatory and Angiogenic Effects Associated with Endometriosis

Evidence shows that LXA4 attenuates pro-inflammatory and angiogenic effects associated with endometriosis. In an experimental study, LXA4 reduced the expression of COX-2 [32,35] and PGE2 levels in endometriotic lesions and peritoneal fluid cells [32]. LXA4 reduced pro-inflammatory cytokines in lesions, ESCs and peritoneal fluid cells during in vivo and in vitro experiments. Among the studied cytokines, treatment with LXA4 reduced the expression of interleukine 1β (IL-1β), interleukin 6 (IL-6), interleukin 10 (IL-10), interleukin 16 (IL-16), vascular endothelial growth factor (VEGF), TNF, transforming growth factor (TGF)-β1 and TGF-β2 [19,27,29,31–33].
