| Abstract: | 肝臟在人體中佔有非常重要的生理功能。而肝病堪稱為台灣人的國病，肝臟病變一般可分為三大階段 : 肝炎、肝硬化、肝癌。非酒精性脂肪肝疾病(nonalcohol fatty liver disease，NAFLD)在臨床症狀表徵及組織病理學上非常類似酒精性肝疾病 （alcoholic fatty liver disease，AFLD），但NAFLD罹患者偶而或絕無長期多量飲酒的不良嗜好。二手菸是一種被動吸菸方式。也是目前危害最廣泛、最嚴重的室內空氣污染，也是全球重大死亡原因。有文獻指出，二手菸會促使循環血液中脂肪的改變，也有可能促使脂肪堆積於肝臟，造成非酒精性脂肪肝疾病。Lumbrokinase是一種血栓溶解酵素，可以直接溶解血栓實體的纖維素，不會有內出血的副作用，也不會溶解具有止血功能的纖維素蛋白原，攝取過剩的Lumbrokinase 會自然排出體外。到目前為止，Lumbrokinase被證實不僅可以治療由血栓引起的心肌梗塞、腦溢血，對於其他各種生活習慣病也具有一定的療效。因此，我們想要了解，Lumbrokinase對於肝臟受損是否也具有一定療效。實驗設計上，我們使用雄性倉鼠作為研究對象，使其暴露於二手菸環境下，再給予Lumbrokinase，以western blot 去分析雄性倉鼠肝臟細胞中凋亡路徑相關蛋白表現情形。實驗結果發現，Lumbrokinase可減少外在細胞凋亡路徑FADD與t-Bid的表現，也可以降低內在細胞凋亡路徑中pro-apoptosis蛋白 Bax/Bad 的表現，而維持anti-apoptosis蛋白Bcl-2穩定表現。同時，當內質網系統受到壓力時，也會活化細胞凋亡路徑。在實驗中同樣發現Lumbrokinase可降低內質網凋亡路徑相關蛋白GADD153與Caspase-12的表現量。由此這些實驗結果可以得知，Lumbrokinase確實可以減緩肝臟細胞暴露於二手菸傷害後所誘導的細胞凋亡路徑造成肝臟細胞死亡。於是，在這裡我們了解到肝臟在受到二手菸的傷害下有疑似發生非酒精性脂肪肝疾病，而目前非酒精性脂肪肝疾病的藥物治療上並無有效的療效。所以，Lumbrokinase未來也許可以提供在非酒精性脂肪肝疾病的治療上的另一個選擇。
Liver plays a very important physiological functions in the human body. Liver disease called the national disease of the Taiwanese. Liver disease generally can be divided into three stages: hepatitis , hepatocirrhosisa and liver cancer. Non-alcoholic fatty liver disease is very similar to alcoholic liver disease on the clinical symptoms Characterization and histopathological ,but NAFLD suffer from occasional or no long-term large amounts of alcohol. Secondhand smoke is a way of passive smoking. It is also against the most extensive, the most serious indoor air pollution, but also the world's major causes of death. Literature, second-hand smoke will lead to a change in the circulating blood fat, may promote fat accumulation in the liver, resulting in non-alcoholic fatty liver disease. Lumbrokinase is a thrombolytic enzyme. It can dissolve blood clots entity cellulose, internal bleeding side effects, does not dissolve the hemostasis cellulose fibrinogen. The uptake surplus Lumbrokinase will naturally excreted. So far, Lumbrokinase was confirmed that not only can be treated by blood clots caused by myocardial infarction, stroke, also have some efficacy for a variety of other lifestyle-related diseases. Therefore, we want to know Lumbrokinase liver damage if a certain effect. On experimental design, we use the male hamster , so that exposure to secondhand smoke, and then give Lumbrokinase, western blot analysis of the apoptotic pathway-related protein expression in the male hamster liver cells circumstances. The experimental results show that, the Lumbrokinase can reduce the performance of the extrinsic apoptotic protein FADD and t-Bid, and can also reduce the intrinsic apoptotic pathway, pro-apoptosis protein Bax / Bad performance, while maintaining the anti-apoptosis protein Bcl-2 stable performance. The same time, when the endoplasmic reticulum under pressure, also activated the apoptotic pathway. In the experiment, the same found Lumbrokinase can reduce the apoptotic pathways of the endoplasmic reticulum protein GADD153 and Caspase-12 expression. Thus these results can be learned, Lumbrokinase really can slow the liver cells exposed to the apoptotic pathway induced by the second-hand smoke damage caused by liver cell death. So, here we learned that the liver in suspected non-alcoholic fatty liver disease, nonalcoholic fatty liver disease drug treatment is not effective the efficacy of passive smoking damage. Therefore, the Lumbrokinase the future may be able to provide another option in the treatment of nonalcoholic fatty liver disease. |
