Polycystic Ovarian Syndrome (PCOS) is a common gynecological endocrine disorder that severely affects the reproductive health of women of reproductive age. Metformin (Met) is currently widely used in clinical practice; however, its application is still limited by certain side effects. Hesperetin (HSP), a natural flavonoid compound, exhibits antioxidative and anti-inflammatory properties, but its effects on ovarian fibrosis in PCOS and the underlying mechanisms remain unclear. This study aimed to investigate the therapeutic effects of HSP on ovarian fibrosis in letrozole-induced PCOS rats and to elucidate its regulatory mechanism involving the TGF-β/Smads signaling pathway. After intervention, body weight, estrous cycle, ovarian histopathological changes (HE and Masson staining), sex hormone levels, lipid profiles, oxidative stress indicators, and insulin resistance index (HOMA-IR) were evaluated. In addition, qRT-PCR and Western blot analyses were performed to assess mRNA expression of antioxidant-related genes and protein expression of the TGF-β/Smads signaling pathway. The results showed that HSP significantly reduced body weight in rats (P < 0.05), restored estrous cyclicity, and improved polycystic ovarian morphological changes. Both low- and high-dose HSP treatments decreased serum testosterone (T) levels (15.70% and 32.92%, respectively) and LH/FSH ratios (69.45% and 77.05%, respectively), while increasing estradiol (E2) levels (1.32-fold and 1.28-fold, respectively). HSP also improved dyslipidemia and insulin resistance, as evidenced by reduced HOMA-IR (39.14% and 42.97%, respectively), and alleviated oxidative stress. Mechanistically, HSP inhibited abnormal activation of the TGF-β/Smads signaling pathway and downregulated the expression of α-SMA and CTGF, thereby attenuating ovarian fibrosis. These findings suggest that HSP may exert therapeutic effects against PCOS-associated ovarian fibrosis by modulating the TGF-β/Smads pathway, providing a theoretical basis for its potential as a therapeutic agent.