论文部分内容阅读
目的研究扇贝多肽(polypeptide from Chlamys farreri,PCF)对紫外线B(UVB)辐射损伤小鼠胸腺淋巴细胞后PI3K/Akt和ASK1-JNK信号通路的影响。方法UVB辐射小鼠胸腺淋巴细胞,用比色法测定胸腺淋巴细胞活性氧(reactive oxygen species,ROS)水平;western-blot检测Akt的活性,预先加入或不加入PI3K/Akt通路特异性抑制剂LY294002检测细胞凋亡信号调节激酶Ⅰ(apoptosis signal regulating kinase-1,ASK1)、JNK的活性、线粒体膜电位(ΔψМ)和DNA ladder。结果PCF能激活AKT的活性,抑制UVB对小鼠胸腺淋巴细胞ASK1凋亡通路的活化。结论PCF通过降低细胞内活性氧的含量,提高AKT的活性,引起ASK1的降解,导致ASK1-JNK诱导的细胞凋亡抑制。
Objective To study the effect of polypeptide from Chlamys farreri (PCF) on the PI3K/Akt and ASK1-JNK signaling pathways after thymocyte injuried by UVB radiation in mice. Methods UVB irradiation of mouse thymocytes was performed. The thymocyte lymphocyte reactive oxygen species (ROS) levels were determined by colorimetry. The activity of Akt was detected by western-blot, with or without PI3K/Akt pathway inhibitor LY294002. Apoptosis signal-regulated kinase-1 (ASK1), JNK activity, mitochondrial membrane potential (ΔψM), and DNA ladder were detected. Results PCF activated AKT activity and inhibited the activation of ASK1 apoptotic pathway in mouse thymic lymphocytes by UVB. Conclusion PCF can increase the activity of AKT by decreasing the content of reactive oxygen species in the cells, causing the degradation of ASK1, leading to the inhibition of ASK1-JNK-induced apoptosis.