.扇贝多肽对UVB辐射诱导HaCat细胞凋亡的抑制作用及其机制[J].中国海洋药物,2006,25(1):16-20.
扇贝多肽对UVB辐射诱导HaCat细胞凋亡的抑制作用及其机制
Inhibitory effects of polypeptides from Chlamys farreri (PCF) on HaCaT cells apoptosis induced by UVB radiation
投稿时间:2005-07-25  
DOI:
中文关键词:  扇贝多肽,中波紫外线,HaCat细胞,凋亡,丝裂原激活的蛋白激酶
English Keywords:polypeptides from Chlamys farreri(PCF),ultraviolet B rays,HaCat cells,apoptosis,mitogen-activated protein kinases
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中文摘要:
      目的建立中波紫外线对体外培养的HaCat细胞辐射损伤病理模型,探讨扇贝多肽(PCF)对HaCat细胞辐射损伤的保护作用及机制。方法将培养的HaCat细胞分组并给予相应的药物,经UVB照射后,琼脂糖凝胶电泳观察各组的DNA ladder;流式细胞仪检测细胞内Caspase-3的含量;Western-blot检测ERKs,JNKs和p38的水平。结果PCF能减少UVB所致的HaCat细胞DNA片段的出现,减少UVB诱导的HaCat细胞内的Caspase-3的含量,还能提高ERKs的水平,但降低JNKs及p38的水平。结论PCF能抑制UVB辐射诱导的细胞凋亡,对UVB辐射损伤的细胞具有保护作用。其作用机制可能是通过调节MAPKs的信号通路和Caspase级联实现。
English Summary:
      Objective To investigate whether PCF could inhibit apoptosis of HaCat cells induced by ultraviolet B(UVB) in vitro and explore its related mechanism.Methods HaCat cells were cultured and divided into groups(control,model,and test groups).The DNA ladder of each group was observed by gel electrophoresis;The expression of caspase-3 in HaCat cells was detected by flow cytometry and the activities of ERKs,JNKs,P38 were determined by western-blot method.Results PCF decresded UVB-induced DNA ladder in HaCat cells;PCF enhanced the level of ERKs,but reduced the level of JNKs and p38,and reduced the expression of Caspase-3 in HaCat cells.Conclusion PCF had protective effects against UVB-induced apoptotic cell death in HaCat cells and it is likely that its cytoprotective effect on HaCat cells was mediated by MAPKs pathway.
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