摘要
目的:探讨ERK信号通路在内质网应激时由A类清道夫受体(SR-A)介导的细胞凋亡中的作用。方法:ERK磷酸化和葡萄糖相关蛋白78(GRP78)的表达用Western blot方法检测,细胞活性用四甲基噻唑蓝(MTT)实验检测,同时应用Annexin V FITC/PI双染流式细胞术检测细胞凋亡率。结果:Western blot结果显示,fucoidan可以持续激活ERK,并且在1～4h达到最强,这种作用在SR-A基因敲除小鼠的腹腔巨噬细胞中明显减弱。用PD98059阻断ERK信号途径后,内质网应激时fucoidan诱导RAW264.7细胞凋亡率明显降低。结论:在发生内质网应激时,fucoidan与SR-A结合后激活ERK信号通路,可能是促进巨噬细胞凋亡的机制之一。
Objective：To investigate the effects of ERK signaling passway on the class A scavenger receptor（SR-A）-mediated apoptosis in the endoreticulum stessed macrophages. Methods：The expression of phosphorylation of ERK1/2 and GRP78 was measured by Western blot;MTF analysis was used to detect the surviving fraction of RAW264.7 cells treated with different concentrations of PD98059;and apoptosis rates of RAW264.7 cells were observed by flow cytometry after staining of Annexin V FITC/PI. Results：Fucoidan continuously activated p-ERK, and the expression of p-ERK kept on peak level through 1 to 4 hours,but was low in the SR-A gene knockout macrophages. Under ER stress,fucoidan-induced apoptosis rates of RAW264.7 cells were significantly decreased by PD98059. Conclusion：These results demonstrated that under ER stress, fucoidan could activate the ERK pathway through SR-A;and activation of p-ERK could contribute to the apoptosis of macrophages.
出处
《南京医科大学学报（自然科学版）》
CAS
CSCD
北大核心
2010年第6期731-735,共5页
Journal of Nanjing Medical University(Natural Sciences)
基金
国家自然科学基金重点项目(30730044)
