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The primary aim of this study is to elucidate the molecular mechanisms underlying CP-induced ovarian injury, with a focus on oxidative stress, inflammatory signaling, and apoptotic pathways, focusing on nuclear factor-kappa B (NF-B), nuclear factor erythroid-2-related factor 2/heme oxygenase-1 (Nrf2/HO-1), Toll-like receptor 4 (TLR4), nucleotide-binding oligomerization domain-like receptor family pyrin domain-containing 3 (NLRP3) inflammasome, silent information regulator-1 (SIRT1), and other signaling pathways involved in the pathogenesis of ovarian injury caused by CP

Additional exploratory endpoints for which data are not reported were: permanent discontinuation of trial product between baseline and week 104