| Summary: | 碩士 === 中山醫學大學 === 生化暨生物科技研究所 === 100 === Second-hand smoke and tobacco smoke products are recognized global risks for human health. It can cause cardiovascular disease and cancer that exposure of second- hand smoke, especially pregnant women and fetus. Several studies have shown an effect of second hand smoke exposure during pregnancy upon lung function in the newborn infant and after birth. However, it is less explored that the liver damage of second-hand smoke exposure. The liver is an exceptional organ in terms of its metabolic, synthetic, and detoxifying function. Recent reports has referred the relationship between second-hand smoke and non-alcoholic fatty liver disease, but not include the liver damage in fetus.
In our experiment, we want to understand affect and explore mechanism about that the fetal liver exposure of second-hand smoke. Experimentally, using hamster fetus, in the injury of secondhand smoke treatment , respectively by gelatin zymography and Western blot observation of hamster fetus liver protein expression in case. The results showed that exposure of second- hand smoke can increase the release of MMP-9, CRP, iNOS , other inflammatory factors and IL-1β in the liver, and lead to increase inflammatory response. It can also be NF-κB activation through P38, AKT and ERK signaling pathways to regulate the inflammatory response,. As well as a significant increase in cell lipid peroxidation and ROS injury degree , so that the immune inflammatory reaction of liver in progress. Meanwhile, the second-hand smoke also can make liver cells to induce apoptosis by the performance of p53/21 protein, and increase oxidative stress thereby enabling the liver lipid accumulation. It belongs to non-alcoholic fatty liver disease in diseases classification . There is no effective drug available for treatment in clinical practice. Therefore, observe inflammation message path of hamster fetal liver. So future we can find a treatment method and reduce second-hand smoke damage to the fetal liver.
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