Polycystic ovary syndrome (PCOS) is the most common cause of women's
infertility. Some inflammatory pathways play a pivotal role in the pathogenesis of PCOS. This study aimed to investigate the possible beneficial effects of
minocycline on
chemokine-like receptor 1 (CMKLR1) and
Insulin Receptor (INSR) in a PCOS model. A molecular docking study was implemented using Molecular Operating Environment (MOE) software. The PCOS was induced in NMRI mice (mean
body weight 14.47±0.23) by 28 days
estradiol valerate injection (2 mg/kg/day). The mice were then divided into six groups (n=8 per group, mean
body weight 17.77± 0.26): control (received
normal saline), PCOS model, control for
minocycline,
minocycline treated PCOS (50 mg/kg),
letrozole treated PCOS (0.5 mg/kg), and
metformin-treated PCOS (300 mg/kg). Serum FSH, LH,
estradiol (E2), and
testosterone were detected by ELISA. The ovarian tissues were stained by
hematoxylin and
eosin. The CMKLR1 and INSR expression levels were determined by Real-time-PCR. The molecular docking studies showed scores of -10.92 and -9.30 kcal/mol, respectively, for
minocycline with CMKLR1 and INSR.
Estradiol valerate treatment led to a significant increase in E2, graffian follicle, and decrease in corpus luteum (CL) numbers (P<0.05), while
minocycline treatment improved these PCOS features. The
minocycline treatment significantly decreased the CMKLR1 expression and increased the INSR expression (P<0.05) while the CMKLR1 expression was increased in PCOS model.
Minocycline may improve ovulation in PCOS model by returning E2 to a normal level and increasing CL number (ovulation signs). These beneficial outcomes may be related to the changes in CMKLR1 and INSR gene expression involved in
glucose metabolism and
inflammation.