Document Type : Original Article
Department of Biology, Damghan Branch, Islamic Azad University, Damghan, Iran
School of Biology, Damghan University, Damghan, Iran
Department of Chemistry, Damghan Branch, Islamic Azad University, Damghan, Iran
Background: Although there are numerous animal models of polycystic ovary syndrome (PCOS), they often fail to
accurately replicate the reproductive and metabolic phenotypes associated with PCOS. The objective of this study is
to assess oxidative status and inflammatory levels in a rat model of PCOS subjected to a new high-fat diet (HFD) in
combination with letrozole.
Materials and Methods: In this experimental study, mature, six-week-old female Sprague-Dawley rats (n=20) were
divided into four groups: control (standard diet); letrozole (letrozole plus a standard diet); HFD; and letrozole+HFD.
After 16 weeks, the rats underwent vaginal smear analysis, measurement of hormonal and lipid profiles, and an
oral glucose tolerance test (OGTT). Ovarian tissue morphology, oxidative parameters, and inflammatory status were
Results: The experimental groups exhibited anoestrus profiles in the vaginal smears and abnormal ovarian morphology,
which was not observed in the control group. Steroid hormone levels were significantly higher in the
letrozole+HFD group compared to the other groups (P=0.00). The experimental groups also showed abnormal glucose
levels and lipid metabolism. The relative expression levels of inflammatory genes were significantly elevated in
the experimental groups compared to the control group (P=0.00), and the letrozole+HFD group exhibited the highest
expression level (P=0.00). The HFD, letrozole, and letrozole+HFD groups demonstrated significantly increased levels
of malondialdehyde (MDA) and reactive oxygen species (ROS), while the levels of enzymatic antioxidants were
significantly reduced compared to the control group (P=0.00).
Conclusion: The combination of a new HFD and letrozole treatment induces inflammation and oxidative stress (OS)
in a rat model of PCOS. This model accurately exhibits abnormal metabolic phenotypes and disruptions in hormonal
profiles associated with PCOS.