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Int. J. Mol. Sci. 2017, 18(12), 2538;

Protective Effects of Liquiritigenin against Citrinin-Triggered, Oxidative-Stress-Mediated Apoptosis and Disruption of Embryonic Development in Mouse Blastocysts

Department of Obstetrics and Gynecology, Taoyuan General Hospital, Ministry of Health & Welfare, Taoyuan City 33004, Taiwan
Department of Bioscience Technology and Center for Nanotechnology, Chung Yuan Christian University, Chung Li District, Taoyuan City 32023, Taiwan
Department of Medical Research, China Medical University Hospital, China Medical University, Taichung 40402, Taiwan
Author to whom correspondence should be addressed.
Received: 27 October 2017 / Revised: 24 November 2017 / Accepted: 24 November 2017 / Published: 27 November 2017
(This article belongs to the Section Biochemistry)
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The mycotoxin citrinin (CTN), a natural contaminant in foodstuffs and animal feeds, exerts cytotoxic and genotoxic effects on various mammalian cells and embryos. A previous investigation by our group revealed potentially hazardous effects of CTN on mouse oocyte maturation and pre- and post-implantation embryo development via the induction of apoptosis. The present study showed that CTN induces apoptosis and inhibits cell proliferation in the inner cell mass of mouse blastocysts. Notably, we observed for the first time that both these effects are suppressed by liquiritigenin (LQ). LQ is a type of flavonoid isolated from Glycyrrhiza radix with several biochemical and pharmacological activities, including antioxidant and anti-inflammatory properties. The preincubation of blastocysts with LQ clearly prevented CTN-induced disruption of pre- and post-implantation embryonic development and fetal weight loss, both in vitro and in vivo. CTN-induced damage processes directly promoted reactive oxygen species (ROS) generation, loss of mitochondrial membrane potential (MMP) and activation of caspase-9 and caspase-3, which were effectively blocked by LQ. Moreover, in an animal model, intravenous injection of dams with CTN (3 mg/kg/day) triggered apoptosis of blastocysts, disruption of embryonic development from the zygote to the blastocyst stage and a decrease in fetal weight. Pre-injection with LQ (5 mg/kg/day) effectively reduced apoptosis and impaired the cytotoxic effects of CTN on development. Our in vivo findings further confirm that CTN exposure via injection has the potential to impair pre- and post-implantation development, leading to apoptosis and the suppression of sequent embryonic development, which can be effectively prevented by LQ. View Full-Text
Keywords: liquiritigenin; citrinin; oxidative stress; apoptosis; embryonic development liquiritigenin; citrinin; oxidative stress; apoptosis; embryonic development

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Huang, C.-H.; Chan, W.-H. Protective Effects of Liquiritigenin against Citrinin-Triggered, Oxidative-Stress-Mediated Apoptosis and Disruption of Embryonic Development in Mouse Blastocysts. Int. J. Mol. Sci. 2017, 18, 2538.

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