Dissertation
Dissertation > Biological Sciences > Cell Biology > Cell physiology > Cell aging and death

Studies on the Inhibitory of Vitamin E in UV Irradiation-induced Cell Apoptosis from Beijing Fatty Chicken

Author CongYiMei
Tutor GuanWeiJun
School Chinese Academy of Agricultural Sciences
Course Animal Genetic Breeding and Reproduction
Keywords vitamin E ultraviolet radiation fibroblast cell apoptosis
CLC Q255
Type Master's thesis
Year 2008
Downloads 69
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In this paper, Using Beijing oil chicken embryos for materials and tissue culture method for adherent cell culture, System described in the ultraviolet radiation-induced oil chicken fibroblast cell apoptosis in the course of vitamin E on apoptotic cell. MTT method of cell proliferation detection, Annexin V-EGFP/PI detection of phosphatidylserine combination of strength, Rh-123 test mitochondrial membrane potential changes, FCM detection of changes in the cell cycle, RT-PCR detection of the bcl-2, bax, fas, caspase-3 gene mRNA level changes. The results are as follows:1. The effect of UV on fibroblast apoptosis is obvious, but also time-dependent, the longer the exposure time, the more obvious effects of apoptosis, but to a certain extent, the cells stop growing, died. Vitamin E could inhibit apoptosis, the greater concentration,the more obvious of inhibition, but when up to a certain extent, the cell viability of the drug group is lower than the control group, showing that vitamin E on the inhibition of apoptosis is a certain Within the limits of the extent, over the extent, will lead to cell death.2. This experiment through quantitative analysis showed that vitamin E has a stronger role in the suppression of apoptosis. The role of vitamin E, through Annexin V-EGFP tag with FCM found that the apoptotic proportion has decreased. And, with the extension of cell culture, vitamin E inhibit the effect of enhancing apoptosis.3. This study used Rh-123 tagged with FCM found that vitamin E in the role of UV-induced apoptosis in cells, the mitochondrial membrane potential increase. However, with training time of mitochondrial membrane potential gradually decreased. It can be speculated that vitamin E inhibited apoptosis with the mitochondria involved in the process.4. This experiment through the detection of vitamin E in the role of UV-induced apoptosis of the cell cycle, found that the ultraviolet radiation of the cell block S phase, leading to G2 / M phase of the reduction. The vitamin E can deal with the down turn of ultraviolet radiation-induced S-phase arrest, caused G2 / M phase of the increase. Cells in the G2 / M ratio improved to allow cell mitosis in the past have more time to repair. Vitamin E is the result of processing cells in the G2 / M phase of accumulation, vitamin E may control the allocation of the cell cycle to play the role of anti-apoptosis.5. RT-PCR results showed that after the UV, bcl-2 gene had no significant change, bax, fas, caspase-3 gene expression increased significantly than the control group, bax/bcl-2 increased. After the accession of vitamin E, bcl-2, caspase-3 gene expression increased significantly than the control group, and bax, fas gene had no significant change, bax/bcl-2 lower. This shows that ultraviolet radiation may be through mitochondrial and death receptor way to induce apoptosis, and the role of vitamin E, may cause a cascade of Caspase family, Bcl-2 family improved up the bcl-2 gene expression to inhibit apoptosis.

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