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BFGF Protective Effects On Oxidative Stress Injury In Mouse Embryo Induced By Trionitropionic Acid

Posted on:2022-01-18Degree:MasterType:Thesis
Country:ChinaCandidate:W TianFull Text:PDF
GTID:2480306338955849Subject:Animal husbandry
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Nowadays,the concept of gender equality has been deeply rooted in people's minds.More and more women are juggling family and work,which brings with it increasing pressure,leading to an increasing incidence of reproductive diseases caused by oxidative stress.Studies have shown that oocyte and embryo quality are reduced due to oxidative stress in the ovary,and the development ability of early embryos is also affected.Therefore,the establishment of the relevant oxidative stress model is of great significance to the research in this field.As an inhibitor of mitochondrial complex ?,3-nitropropionic acid(3-NPA)can inhibit cellular mitochondrial function by 3-nitropropionic acid,resulting in a lack of cellular ATP.3-nitropropionic acid can also induce mitochondrial production and release of ROS,so cellular oxidative stress is induced.In this study,a mouse ovarian oxidative stress model was established by intraperitoneal injection of 3-nitropropionic acid(3-NPA).Basic fibroblast growth factor(bFGF)is a CATionic peptide containing 155 amino acids that promotes mitosis and can repair tissue cells and promote proliferation and differentiation of tissue cells.BFGF also has a certain effect on oxidative stress and inhibition of apoptosis.The purpose of this study was to investigate the effects of the addition of basic fibroblast growth factor(bFGF)to the medium in vitro on the development of3-nitropropionic acid-induced mouse early embryos in vitro.(KSOM)test is divided into negative control group,positive control group(KSOM + bFGF),3-NPA treatment group(injected with 3-NPA + KSOM),antioxidant treatment group(KSOM+ 3-NPA injection + bFGF)in the body,of the four experimental mouse blastocyst stage embryos inside the active oxygen content,glutathione levels and mitochondrial membrane potential detection and analyzed,and then within the blastocyst stage embryos each test group on oxidation resistance related gene SOD1,SOD2,GPX3,GPX4,CAT,the Nrf,The m RNA expression levels of SOX2,CDX2 and H19 genes related to totipotency and Bax,Cyt-c and Caspase-9 genes related to apoptosis were also detected.The results showed that compared with the blank control group,the 4-cell rate and blastocyst rate in 100 ng/m L bFGF treatment group were significantly increased(P < 0.05).Therefore,100 ng/m L bFGF was the optimal treatment concentration.At the same time,bFGF significantly decreased the content of reactive oxygen species in blastocyst embryos(P < 0.05),and significantly increased the level of glutathione and mitochondrial membrane potential in blastocyst embryos(P < 0.05).The m RNA expression levels of antioxidant genes GPX3,GPX4,NRF2,SOD1,SOD2 and CAT in blastocyst embryos were upregulated after the addition of bFGF in the culture medium of early mouse embryos in vitro.In addition,the addition of bFGF also increased the m RNA expression levels of totipotency related genes SOX2,CDX2 and H19 in blastocyst embryos.Finally,it was found that the addition of bFGF also decreased the m RNA expression levels of apoptosis related genes Bax,Cyt-c and Caspase-9 in blastocyst embryos.These results showed that bFGF by reducing the early embryo in mice induced by 3-nitro propionic acid oxidative stress levels and improve the level of mitochondrial membrane potential,thus raising the 3-nitro propionic acid induced antioxidant levels of early embryo in mice and reduced the level of cell apoptosis,and effectively protect the 3-nitro propionic acid induced mouse early embryos development in vitro,improved 3-the quality of early embryo in mice induced by nitro propionic acid.
Keywords/Search Tags:Mouse, bFGF, Embryo development in vivo, 3-NPA, NRF2 gene
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