NFKB1 and polycystic ovary syndrome: Subsequent in vivo validation demonstrated that BSTJF ameliorates GC dysfunction in PCOS likely through targeting the AGEs-RAGE axis to suppress NOX4 activation, leading to inhibition of p38 MAPK phosphorylation and NF-κB nuclear translocation, ultimately alleviating ovarian oxidative and inflammatory stress (Fig. 10E).