The quality of oocytes in patients with polycystic ovary syndrome (PCOS) decreases, which is closely related to the function of oocytes' mitochondria. If mitochondrial dysfunction is involved in PCOS, it is likely to affect the function of cumulus cells. However, the mechanism of mitochondrial dysfunction remains unclear. In the present study, granulosa cells were collected from women attending the Hebei Reproductive Health Hospital and were divided into the normal ovarian reserve group (CON group) and the PCOS group. The mitochondrial ultrastructure was observed by transmission electron microscope, and the mitochondrial function was determined by detecting the ATP content, reactive oxygen species levels, the number of mitochondria and the mitochondrial membrane potential. Additionally, western blotting was used to compare the expression levels of mitochondrial kinetic protein, the related channel protein, between the two groups. In the present study, it was found that patients with PCOS had abnormal granulosa cell morphology, increased mitochondrial abnormalities, decreased mitochondrial function and disturbed mitochondrial dynamics. In addition, the silent information regulator 1/phosphorylated‑AMP‑activated protein kinase/peroxisome proliferator‑activated receptor‑γ coactivator 1α pathway expression was decreased, and it was hypothesized that the decreased mitochondrial mass in the PCOS group was associated with it.
Keywords: mitochondria; mural granulosa cells; peroxisome proliferator-activated receptor‑γ coactivator 1α; polycystic ovary syndrome; silent information regulator 1.