蚓酵素減緩二手菸及老化所誘發倉鼠肝損傷之研究

血栓為心血管疾病的直接死亡原因之一。血管隨著年齡的增長而老化，同時不良的生活習慣，會帶來血管的生理與機能的衰退，而造成血管的病變。研究發現，來自於Lumbricus Rubellus的腸和體液中含有和尿酸素一樣具有溶解纖維素機能的酵素-命名為Lumbrokinase。Lumbrokinase 可以成功的代替urokinase或t-PA等纖維素溶解酵素活化劑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。Lumbrokinase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，在這裡我們想要去了解Lumbrokinase在肝臟受損的情況下，使否也具有等同的效果。實驗上，使用倉鼠做為研究的對象，在secondhand smoke的傷害下去處理Lumbrokinase，以zymography及western blot去分別觀察年輕及老化倉鼠的肝臟中蛋白的表現情形，結果發現Lumbrokinase可以明顯的減少肝臟中MMP-9、CRP、iNOS等發炎因子的釋放，而有效的降低發炎反應，也可以透過膜上的Toll-like receptor(TLR)，經由MyD88、P38、JNK、MAPK 等訊息路徑去活化NFκ-B而調節免疫系統，減少IL-6、TNF-α、IL1-β的產生，以及顯著的改善細胞脂質過氧化、ROS傷害的程度，達到減緩肝臟中免疫發炎反應的目的。同時，Lumbrokinase也可藉由調控p53/21蛋白的表現進而抑制二手菸所誘發的細胞凋亡的情形。於是，在這裡我們發現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。

Thrombosis direct causes of death is cardiovascular disease. Vascular aging as you grow older, and bad living habits, will result in vascular Physiology and function of the recession, caused by vascular lesions. Study finds that comes from Lumbricus Rubellus in the gut and body fluid containing dissolved cellulose and effect of uric acid as a function of the enzyme-naming of Lumbrokinase. Instead of urokinase may Lumbrokinase success or t-PA cellulose dissolved cellulose direct thrombolytic enzyme Activator entities, will not have side-effects of hemorrhage, Hemostatic function of cellulose and protein is also not dissolved the original. Lumbrokinase not only in the treatment of myocardial infarction, stroke caused by a thrombus, for various other lifestyle-related disease also has a certain effect. So, here we want to know Lumbrokinase in cases of liver damage, so that it also has the same effect. Experimentally, using hamsters as objects of study, in the harm of secondhand smoke treatment of Lumbrokinase, respectively by zymography and Western blot observation of young and aging of Hamster liver protein expression in case, Results found Lumbrokinase can obvious of reduce liver in the MMP-9, and CRP, and iNOS, inflammation factor of release, and effective of reduce inflammation reaction, also can through film Shang of Toll-like receptor (TLR), through MyD88, P38, JNK, and MAPK, message path to activation NF-B and regulation immune system, reduce IL-6, TNF-α, and IL1-β of produced, and dramatically improved cell lipid peroxidation, ROS injury degree, reached slowed liver in the immune inflammation reaction of purpose. Meanwhile, Lumbrokinase may, by regulation and expression of p53/21 protein in turn inhibits apoptosis induced by second-hand smoke. So, here we find that the damage to the liver in second-hand smoke have suspected occurrence under non-alcoholic fatty liver disease, and non-alcoholic fatty liver disease and no effective curative effect of drug treatment, so future may Lumbrokinase provided on treatment of nonalcoholic fatty liver disease in another option.