MMP-9 dysregulation and chronic inflammation in polycystic ovary syndrome: linking ovulatory dysfunction to diagnostic implications.

BACKGROUND: Dysregulation of matrix metalloproteinase 9 (MMP-9) and chronic low-grade inflammation have been implicated ovulatory dysfunction in polycystic ovary syndrome (PCOS), yet their roles remain inadequately addressed in clinical practice. This study aimed to investigate the interrelationships and functional roles of inflammation, hormone, and the MMP-9/TIMP-1 system in PCOS. METHOD: A PCOS rat model was established to evaluate serum hormone levels, inflammatory markers, and MMP-9/TIMP-1 levels. Ovarian expression of IL-6 and MMP-9 was examined using Immunohistochemistry and immunofluorescence. Additionally, a cohort study comprising 83 PCOS patients and 97 healthy controls was analyzed to evaluate serum hormonal and inflammatory profiles, with further assessment of their associations with PCOS and predictive value. RESULT: In the PCOS rat model, marked disruptions in serum lipid and hormone profiles were observed, accompanied by elevated levels of IL-6 and MMP-9. Histological examination of ovarian tissues showed an increased number of atretic follicles and enhanced expression of both IL-6 and MMP-9. In the clinical cohort, patients with PCOS showed significantly higher levels of TSTO, LH and IL-6 compared to controls. Although MMP-9 and TIMP-1 levels were both elevated, the MMP9/TIMP1 ratio remained unchanged. Correlation analysis indicated positive associations between IL-6, TNF-α, MMP-9, TIMP-1, and PCOS. Logistic regression identified TSTO, FSH, and IL-6 as independent risk factors, with ROC analysis further highlighting IL-6 as the most robust predictor for PCOS. CONCLUSION: This study demonstrates that systemic inflammation and hormonal disturbances are closely linked to PCOS. In PCOS patients, particular attention should be given to elevated levels of inflammatory factors such as IL-6 and dysregulated of the immune microenvironment, which play critical roles in the pathogenesis of the disease. Further exploration of the potential application of targeted inflammatory management in clinical intervention strategies is warranted.