CAJ | 학술논문

目的：初步探讨甲壳胺诱导人肝癌HepG2细胞凋亡的信号转导机制。方法：采用酶联免疫法，动态检测甲壳胺作用于HepG2细胞后，细胞膜相及胞浆内的蛋白酪氨酸激酶（PTK）及蛋白酪氨酸磷酸酶（PTP）活性的变化。结果：甲壳胺可以抑制HepG2细胞内的PTK活性，并呈一定的浓度依赖性；甲壳胺作用HepG2细胞后，随着PTK活性的减弱，PTP的活性也短暂下降。结论：甲壳胺诱导HepG2细胞凋亡时，涉及到PTK的活性改变。观察到膜相蛋白中PTK的活性改变早于胞浆蛋白，提示可能存在一个信号的跨膜转运过程；同时伴有PTP的活性变化，可能反映了胞内蛋白酪氨酸残基的磷酸化与去磷酸化即时调节机制。
목적：초보탐토갑각알유도인간암HepG2세포조망적신호전도궤제。방법：채용매련면역법，동태검측갑각알작용우HepG2세포후，세포막상급포장내적단백락안산격매（PTK）급단백락안산린산매（PTP）활성적변화。결과：갑각알가이억제HepG2세포내적PTK활성，병정일정적농도의뢰성；갑각알작용HepG2세포후，수착PTK활성적감약，PTP적활성야단잠하강。결론：갑각알유도HepG2세포조망시，섭급도PTK적활성개변。관찰도막상단백중PTK적활성개변조우포장단백，제시가능존재일개신호적과막전운과정；동시반유PTP적활성변화，가능반영료포내단백락안산잔기적린산화여거린산화즉시조절궤제。
Objective: To investigate the mechanism of signal transduction in apoptosis of HepG2 cells induced by chitosan. Methods: ELISA was used to dynamically detect the activity of protein tyrosine kinase(PTK) and pro?tein tyrosine phosphatase(PTP) in the cytoplasm and the membrane of HepG2 cells treated by chitosan. Results:In HepG2 cells, chitosan inhibited the activity of PTK dose-depended within 1000 mg/L. And companied with the activity of PTK, the activity of the PTP decreased transiently in cells after treated with chitosan. Conclusion: The change of PTK activity is involved in the apoptosis of HepG2 cells induced by chitosan. The PTK activity in cell membrane decreased more rapidly than that in cell cytoplasm, which indicates an existence of a transmembrane signal transduction. And the change of PTP activity following with the PTK suggests the real time regulation of phosphorylation and dephosphorylation.