Elnaz Salahi1, Fardin Amidi1, Ziba Zahiri2, Marziye Aghahosseini3, Farhad Mashayekhi4, Showra Amani Abkenari1, Shirzad Hosseinishenatal1, Aligholi Sobhani5. 1. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Poursina ST, Tehran, Iran. 2. Reproductive Health Research Center, Department of Obstetrics and Gynecology, Alzahra Hospital, School of Medicine, Guilan University of Medical Science, Rasht, Iran. 3. Department of Obstetrics and Gynecology, School of Medicine, Tehran University of Medical Sciences, Tehran, Iran. 4. Department of Biology, Faculty of Sciences, University of Guilan, Rasht, Iran. 5. Department of Anatomy, School of Medicine, Tehran University of Medical Sciences, Poursina ST, Tehran, Iran. sobhania@sina.tums.ac.ir.
Abstract
PURPOSE: Considerable evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the pathogenesis of Polycystic ovary syndrome (PCOS). We aimed to evaluate the effectiveness of mitochondria-targeted antioxidant, MitoQ10, on the redox signaling pathway's component in PCOS. METHOD: We assessed TXNIP, TRX, and ASK1 expression in granulosa cells (GCs) of the DHEA-induced PCOS mouse model. Female BALB/c mice in five groups of Control, DHEA, and DHEA + MitoQ10 in three doses of 250, 500, and 750 μmol/L MitoQ10 were treated for 21 days. RESULTS: Histological investigation showed a probable improvement in folliculogenesis; besides, ASK1 and TXNIP expression were significantly increased in GCs of the PCOS mouse F4Fmodel as compared to the control groups and decreased steadily in groups treated by MitoQ10. However, TRX expression showed a drop that was restored by MitoQ10 meaningfully (P ≤ 0.05). CONCLUSION: The work presented herein suggests mitochondria-targeted antioxidant, MitoQ10, have modulating effects on folliculogenesis in the ovary and also on the redox signaling pathway in GCs of PCOS mouse model which may have potential to attenuate oxidative stress and its relative damages.
PURPOSE: Considerable evidence suggests that mitochondrial dysfunction and oxidative stress contribute to the pathogenesis of Polycystic ovary syndrome (PCOS). We aimed to evaluate the effectiveness of mitochondria-targeted antioxidant, MitoQ10, on the redox signaling pathway's component in PCOS. METHOD: We assessed TXNIP, TRX, and ASK1 expression in granulosa cells (GCs) of the DHEA-induced PCOS mouse model. Female BALB/c mice in five groups of Control, DHEA, and DHEA + MitoQ10 in three doses of 250, 500, and 750 μmol/L MitoQ10 were treated for 21 days. RESULTS: Histological investigation showed a probable improvement in folliculogenesis; besides, ASK1 and TXNIP expression were significantly increased in GCs of the PCOS mouse F4Fmodel as compared to the control groups and decreased steadily in groups treated by MitoQ10. However, TRX expression showed a drop that was restored by MitoQ10 meaningfully (P ≤ 0.05). CONCLUSION: The work presented herein suggests mitochondria-targeted antioxidant, MitoQ10, have modulating effects on folliculogenesis in the ovary and also on the redox signaling pathway in GCs of PCOS mouse model which may have potential to attenuate oxidative stress and its relative damages.
Authors: Carlo Alviggi; Federica Cariati; Alessandro Conforti; Pasquale De Rosa; Roberta Vallone; Ida Strina; Rosario Pivonello; Giuseppe De Placido Journal: Reprod Toxicol Date: 2015-11-03 Impact factor: 3.143