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Mechanisms of Selenium and Vitamin C Inhibition of VSMC Injury Induced by Triol

Author: TangRong
Tutor: HuangKaiXun
School: Huazhong University of Science and Technology
Course: Biomedical Engineering
Keywords: Triol Selenium Vitamin C Vascular smooth muscle cells Oxidative damage Apoptosis Reactive oxygen species Mitochondria
CLC: R543
Type: PhD thesis
Year: 2005
Downloads: 168
Quote: 1
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Abstract


Atherosclerosis (AS) is a serious threat to human diseases, oxidized steroids are considered to be the main causative factor of the AS. Reveal the oxidized steroids cytotoxicity and their role in the pathogenesis of AS, prevention, research and development of AS is still one of the topics at the forefront of the current population and health research areas. Vitamin C and essential trace element selenium (Se) attaches great importance to the people's prevention of AS occurrence and development of function, but the mechanism is not yet very clear. Rat vascular smooth muscle cells (VSMC), vitamin C (Vc) on VSMC growth of oxidized steroids Triol (cholestane-3β-5α-6β-triol) cell damage and supplemental selenium and vitamin C achieved the following results: 1) the application of MTT assay, fluorescence microscopy and DNA gel electrophoresis to study the effects of vitamin C on VSMC growth inhibition mechanism of their injury. The results showed that low doses of vitamin C to promote cell proliferation, while high doses of vitamin C reduce the survival rate of the cells, and induce apoptosis. Further studies have shown that high doses of vitamin C (≥ 500μM) promote oxidation, changes in intracellular reduced state, leading to cellular oxidative damage caused by the decreased activity of antioxidant enzymes GPx and SOD. High doses of vitamin C also stimulates ROS production and intracellular Ca 2 increased concentration, inhibition of bcl-2 mRNA expression, leading to apoptosis. 2) by cell growth curve, MTT assay, GPx, SOD enzyme activity test, lipid over oxidation levels were measured and GPx and TR mRNA expression levels of detection Triol toxicity rat VSMC role and Na SeO 3 of Vc on Triol cytotoxic protective effect. The results showed that the the Triol inhibition of VSMC growth, leading to cellular oxidative damage, caused by the increase in cell GPx and SOD activity decreased cellular lipid peroxide levels, total antioxidant capacity weakened significantly reduced cell viability in a concentration and time, and these effects dependencies. Na 2 the SeO 3 and Vc pre-incubation of cells can effectively help the the VSMC cell resistance Triol toxicity. Na 2, SeO , 3 lipid peroxidation improve increased cell GPx and TR mRNA expression increased cell GPx, SOD enzyme activity, decreased cell damage, improve cell survival . Na 2 SeO 3 protective effect on cells with the extension of the pre-incubation time enhanced. Vc as an antioxidant, can clear Triol induced lipid hydroperoxide, thereby reducing the cellular oxidative damage caused by the Triol, the maintenance of intracellular GPx, SOD enzyme activity, reduce lipid peroxidation injury. Obvious dose-effect relationship of Vc the protective effect on cells, Na 2 the SeO 3 and Vc pre-incubation of cells, both synergistic effect. 3) membrane fluidity was measured by detecting LDH leakage rate, DPH fluorescent probe, AFM directly observed

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CLC: > Medicine, health > Internal Medicine > Heart, blood vessels ( circulatory ) disease > Vascular disease
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