Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos
碩士 === 中原大學 === 生物科技研究所 === 100 === Ginsenosides-Rg1, the most abundant compound found in Asian ginseng (Panax ginseng), has demonstrated pharmacological effects such as neuroprotective, immune-stimulant and anti-diabetic agent. Pregnant women, especially in Asian community, consume the ginseng as n...
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ndltd-TW-100CYCU51110042015-10-13T21:32:34Z http://ndltd.ncl.edu.tw/handle/79260856892435704245 Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos 人參皂苷Rg-1誘導小鼠胚胎發育傷害和內源性細胞凋亡 Rica-Anggelia Madonna 雷安琪 碩士 中原大學 生物科技研究所 100 Ginsenosides-Rg1, the most abundant compound found in Asian ginseng (Panax ginseng), has demonstrated pharmacological effects such as neuroprotective, immune-stimulant and anti-diabetic agent. Pregnant women, especially in Asian community, consume the ginseng as nutritive supplement. Thus, the effects of Ginsenoside-Rg1 on mouse embryo need to be investigated. Moreover, the regulatory mechanisms of Ginsenoside-Rg1 affected mouse blastocyst remains unknown. In this study, we also explored intracellular signaling mechanisms involved in that process. First, the mouse blastocysts were exposed by 25, 50 and 100 µM Ginsenoside-Rg1. Cell viability and proliferation in blastocyst, early embryonic development (in vitro) as well as blastocyst outgrowth were evaluated by TUNEL assay, Hoechst staining and morphological observation under microscope, respectively. Fluorescence staining was performed to observe the apoptosis pathway induced by Ginsenoside-Rg1. The result showed that 100 µM Ginsenoside-Rg1 could induce cell apoptosis and inhibit cell proliferation in mouse blastocyst. Fluorescence staining data revealed that Ginsenoside-Rg1 increased ROS (Reactive oxygen species) production and of Bax/Bcl-2 ratio of mouse blastocyst. That ROS production could be inhibited by NAC (N-Acetyl-Cysteine) pretreatment which lead to cell apoptosis prevention. In addition, Ginsenoside-Rg1 caused loss of MMP (Mitochondrial Membrane Potential) and triggered the activation of caspase-9 and caspase-3, but not caspase-8. Other adverse effects of Ginsenoside-Rg1 were retardation of early embryonic development at 25 µM or more concentration and embryo outgrowth disruption after blastocyst outgrowth (in vitro) at 100 µM concentrations. Taken together, our results showed that the intake of Ginsenoside-Rg1 has potentially hazardous during pregnancy. Furthermore, Ginsenoside-Rg1 exposure promotes cell apoptosis in mouse blastocyst and it occurs through intrinsic pathway. Wen-Hsiung Chan 詹文雄 2012 學位論文 ; thesis 74 en_US |
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碩士 === 中原大學 === 生物科技研究所 === 100 === Ginsenosides-Rg1, the most abundant compound found in Asian ginseng (Panax ginseng), has demonstrated pharmacological effects such as neuroprotective, immune-stimulant and anti-diabetic agent. Pregnant women, especially in Asian community, consume the ginseng as nutritive supplement. Thus, the effects of Ginsenoside-Rg1 on mouse embryo need to be investigated. Moreover, the regulatory mechanisms of Ginsenoside-Rg1 affected mouse blastocyst remains unknown. In this study, we also explored intracellular signaling mechanisms involved in that process. First, the mouse blastocysts were exposed by 25, 50 and 100 µM Ginsenoside-Rg1. Cell viability and proliferation in blastocyst, early embryonic development (in vitro) as well as blastocyst outgrowth were evaluated by TUNEL assay, Hoechst staining and morphological observation under microscope, respectively. Fluorescence staining was performed to observe the apoptosis pathway induced by Ginsenoside-Rg1. The result showed that 100 µM Ginsenoside-Rg1 could induce cell apoptosis and inhibit cell proliferation in mouse blastocyst. Fluorescence staining data revealed that Ginsenoside-Rg1 increased ROS (Reactive oxygen species) production and of Bax/Bcl-2 ratio of mouse blastocyst. That ROS production could be inhibited by NAC (N-Acetyl-Cysteine) pretreatment which lead to cell apoptosis prevention. In addition, Ginsenoside-Rg1 caused loss of MMP (Mitochondrial Membrane Potential) and triggered the activation of caspase-9 and caspase-3, but not caspase-8. Other adverse effects of Ginsenoside-Rg1 were retardation of early embryonic development at 25 µM or more concentration and embryo outgrowth disruption after blastocyst outgrowth (in vitro) at 100 µM concentrations. Taken together, our results showed that the intake of Ginsenoside-Rg1 has potentially hazardous during pregnancy. Furthermore, Ginsenoside-Rg1 exposure promotes cell apoptosis in mouse blastocyst and it occurs through intrinsic pathway.
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author2 |
Wen-Hsiung Chan |
author_facet |
Wen-Hsiung Chan Rica-Anggelia Madonna 雷安琪 |
author |
Rica-Anggelia Madonna 雷安琪 |
spellingShingle |
Rica-Anggelia Madonna 雷安琪 Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos |
author_sort |
Rica-Anggelia Madonna |
title |
Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos |
title_short |
Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos |
title_full |
Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos |
title_fullStr |
Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos |
title_full_unstemmed |
Ginsenoside-Rg1 Exposure Induces Developmental Injury and Intrinsic Apoptotic Pathway in Mouse Embryos |
title_sort |
ginsenoside-rg1 exposure induces developmental injury and intrinsic apoptotic pathway in mouse embryos |
publishDate |
2012 |
url |
http://ndltd.ncl.edu.tw/handle/79260856892435704245 |
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