高糖对ECV304细胞中Cofilin-1表达及PKC活性的影响  被引量:4

Expression of Cofilin-1 and Activity of PKC in High-Glucose Induced ECV304 Cells

在线阅读下载全文

作  者:汪引芳[1] 王凤杰[1] 王念[1] 刘永明[1] 

机构地区:[1]武汉大学医学院病理生理学教研室,湖北武汉430071

出  处:《武汉大学学报(医学版)》2008年第3期328-331,共4页Medical Journal of Wuhan University

摘  要:目的:探讨高糖刺激对ECV304细胞中Cofilin-1的表达及蛋白激酶C(PKC)活性的影响。方法:常规培养ECV304细胞,分组给药后,非放射性酶法检测该细胞中PKC的活性,RT-PCR法检测细胞Cofilin-1总mRNA的表达。结果:经高糖作用后,ECV304细胞PKC活性较低糖的正常组明显增加(P<0.01),细胞内Cofilin-1总mRNA的表达显著增强(P<0.01);而预先给予PKC抑制剂GF109203x处理能显著地抑制高糖介导的ECV304细胞内PKC活性的升高(P<0.01)和胞内Cofilin-1总mRNA的表达(P<0.05),但对正常组PKC活性和Cofilin-1总mRNA的表达无显著性影响。结论:高糖刺激可能通过PKC信号传导通路使Cofilin-1表达增强,进一步导致糖尿病血管病变的发生。Objective: To observe the alteration of the expression of cofilin-1 and the regulative effect of protein kinase C (PKC) in high-glucose induced ECV304 cells. Methods: The ECV304Cells were routinely cultured in L-DMEM medium, and then were treated with different factors. Activity of protein kinase C (PKC) within the cells was detected by Pep Tag assay for non-radioactive detec- tion. Also, the expression of cofilin-1 was detected by RT-PCR assay. Results: The activity of PKC within cells obviously increased (P〈0. 01), and the expression of cofilin-1 significantly strengthened after stimulation of high-glucose on the cells (P〈0.01). At the same time, when the cells were pretreated with GF109203x, the inhibitor of PKC, the activity of PKC within cells which increased formerly by high-glucose was apparently inhibited(P〈0.01), and expression of cofilin-1 was also inhibited(P〈0.05). But GF109203x had no apparent effect on the expression of cofilin-1 and activity of PKC within low-glucose cultured cells. Conclusion: The high-glucose can improve the expression of cofilin-1 through PKC signaling pathway. It may be an important path ogenesis for diabetic vascular complications.

关 键 词:Cofilin-1 蛋白激酶C 高糖 细胞骨架 

分 类 号:R363.2[医药卫生—病理学]

 

参考文献:

正在载入数据...

 

二级参考文献:

正在载入数据...

 

耦合文献:

正在载入数据...

 

引证文献:

正在载入数据...

 

二级引证文献:

正在载入数据...

 

同被引文献:

正在载入数据...

 

相关期刊文献:

正在载入数据...

相关的主题
相关的作者对象
相关的机构对象