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Background: Despite abnormal apoptosis of granulosa cells is believed to have a role in the pathophysiology of polycystic ovarian syndrome (PCOS), the cellular and molecular processes behind this are unknown. Atresia occurs in developing PCOS follicles, likely facilitated by increased androgen levels. Atretic follicles are eliminated in the absence of tissue injury or inflammation, suggesting that programmed cell death may be the mechanism behind this process. Aim of the Study: The current study evaluated the protective effect of L-carnitine (LC) against programmed cell death and, eventually, endometrial receptivity. Patients and Methods: This prospective case-control research was performed at the Al-Nahrain University’s high institute for infertility diagnosis and assisted reproductive technologies and the Al-Farah Specialist Fertility Center. Sixty women diagnosed with the polycystic ovarian syndrome were recruited in this research and began their IVF/ICSI cycle; clusterin and annexin V were measured as apoptotic markers in the early follicular phase of the cycle CD2-in the serum and in the follicular fluid on the day of ova pickup. Endometrial thickness was assessed by ultrasound examination.Results: Both serum annexin V and clusterin were decreased significantly after treatment (p< 0.05). The mean endometrial thickness in all enrolled women was 5.30 ± 0.70 mm. There was no significant difference in mean endometrial thickness between the study and placebo groups, 5.43 ± 0.63 versus 5.37 ± 0.66 mm, respectively (p = 0.441). There was no significant difference in mean serum annexin V (p = 0.101), but follicular fluid annexin V and serum and follicular fluid clusterin were lower in the study group than in the placebo group in a significant manner (p |
