解剖学报
解剖學報
해부학보
ACTA ANATOMICA SINICA
2014年
4期
480-484
,共5页
安建多%江瑛%白云飞%王学江
安建多%江瑛%白雲飛%王學江
안건다%강영%백운비%왕학강
解耦联蛋白2%肝纤维化%星形细胞%p38丝裂素活化蛋白激酶%免疫印迹法%大鼠
解耦聯蛋白2%肝纖維化%星形細胞%p38絲裂素活化蛋白激酶%免疫印跡法%大鼠
해우련단백2%간섬유화%성형세포%p38사렬소활화단백격매%면역인적법%대서
Uncoupling protein 2%Liver fibrosis%Hepatic stellate cells%p38 Mitogen activated protein kinase%Western blotting%Rat
目的：探讨解耦联蛋白2（ UCP2）在肝纤维化形成过程中的作用及其发生机制。方法体内实验采用四氯化碳（CCl4）诱导肝纤维化模型，取肝脏观察病理变化，用Western blotting、免疫组织化学和Real-time PCR等方法检测UCP2和p38丝裂素活化蛋白激酶（ p38MAPK）的表达水平；体外实验采用UCP2特异性抑制剂京尼平和CCl4刺激星形细胞，检测UCP2和p38MAPK相关蛋白的表达情况。结果与正常组相比，模型组大鼠肝脏α-平滑肌肌动蛋白（α-SMA）和UCP2表达增高（P＜0．05，n＝10）；加入CCl4刺激细胞后，星形细胞α-SMA表达增加， p38MAPK及其磷酸化水平增高（P＜0．05，n＝6）；而在加入京尼平后，α-SMA表达增加，p38 MAPK及其磷酸化水平明显降低（P＜0．05，n＝6）。结论 UCP2参与了肝纤维化的发生，可能促进了星形细胞的活化及增殖过程。
目的：探討解耦聯蛋白2（ UCP2）在肝纖維化形成過程中的作用及其髮生機製。方法體內實驗採用四氯化碳（CCl4）誘導肝纖維化模型，取肝髒觀察病理變化，用Western blotting、免疫組織化學和Real-time PCR等方法檢測UCP2和p38絲裂素活化蛋白激酶（ p38MAPK）的錶達水平；體外實驗採用UCP2特異性抑製劑京尼平和CCl4刺激星形細胞，檢測UCP2和p38MAPK相關蛋白的錶達情況。結果與正常組相比，模型組大鼠肝髒α-平滑肌肌動蛋白（α-SMA）和UCP2錶達增高（P＜0．05，n＝10）；加入CCl4刺激細胞後，星形細胞α-SMA錶達增加， p38MAPK及其燐痠化水平增高（P＜0．05，n＝6）；而在加入京尼平後，α-SMA錶達增加，p38 MAPK及其燐痠化水平明顯降低（P＜0．05，n＝6）。結論 UCP2參與瞭肝纖維化的髮生，可能促進瞭星形細胞的活化及增殖過程。
목적：탐토해우련단백2（ UCP2）재간섬유화형성과정중적작용급기발생궤제。방법체내실험채용사록화탄（CCl4）유도간섬유화모형，취간장관찰병리변화，용Western blotting、면역조직화학화Real-time PCR등방법검측UCP2화p38사렬소활화단백격매（ p38MAPK）적표체수평；체외실험채용UCP2특이성억제제경니평화CCl4자격성형세포，검측UCP2화p38MAPK상관단백적표체정황。결과여정상조상비，모형조대서간장α-평활기기동단백（α-SMA）화UCP2표체증고（P＜0．05，n＝10）；가입CCl4자격세포후，성형세포α-SMA표체증가， p38MAPK급기린산화수평증고（P＜0．05，n＝6）；이재가입경니평후，α-SMA표체증가，p38 MAPK급기린산화수평명현강저（P＜0．05，n＝6）。결론 UCP2삼여료간섬유화적발생，가능촉진료성형세포적활화급증식과정。
Objective To explore the role of uncoupling protein 2 ( UCP2) in the development of hepatic fibrosis and its molecular mechanism .Methods The CCl4-induced liver fibrosis rat model in vivo was established to observe the pathological changes of rat livers .The expression levels of UCP2 and p38 mitogen activated protein kinase (p38 MAPK) were detected by using the techniques of Western blotting , Real-time PCR and immunohistochemistry .The hepatic stellate cells ( HSC) were stimulated by CCl 4 and UCP2-specific inhibitor Genipin to mimic liver fibrosis in vitro.The expression levels of UCP2 and p38MAPK were determined by using Western blotting .Results We found that UCP2 and α-SMA expression levels increased significantly (P <0.05, n =10) in the liver of rats with CCl4-induced liver fibrosis when compared with that of the normal control rats in vivo.Similarly, the expression levels of UCP2 and p38 MAPK were up regulated (P <0.05, n=6) in CCl4-treated HSC cells in vitro.However, the expressions of UCP2 and p38 MAPK were down regulated (P <0.05, n=6) in genipin-treated HSC cells in vitro.Conclusion UCP2 is involved in liver fibrosis, and probably contributed to the activation and proliferation of hepatic stellate cells .
