摘要
目的:初步探讨甲壳胺诱导人肝癌Hep G2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Hep G2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Hep G2细胞内的PTK活性,并呈一定的浓度依赖性;甲壳胺作用Hep G2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Hep G2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。
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.
出处
《生物技术通讯》
CAS
2014年第6期846-848,共3页
Letters in Biotechnology
基金
国家自然科学基金(81102410)
