异氟烷对心肌细胞血管内皮生长因子表达的影响

目的:探讨异氟烷对心肌细胞血管内皮生长因子(VEGF)的直接调节作用及其可能的细胞内信号转导途径,揭示异氟烷心肌保护的分子机制。方法:分离培养原代大鼠心肌细胞,随机分为:对照组(CON),细胞不经任何处理;异氟烷组(ISO),细胞分别经0.5、1、1.5MAC的异氟烷处理6h;PKC抑制剂组(CAL),细胞经calphostinC 50nM孵育6h;PKC抑制剂+异氟烷组(IC),细胞经calphostin C及异氟烷共同作用6h。实验结束采用E1isa法测定细胞培养液VEGF浓度。结果:异氟烷呈浓度依赖性增加心肌细胞VEGF分泌,与对照组(OMAC)比较,1MAC和1.5MAC组VEGF值均显著升高(P<0.01);PKC抑制剂calphostin C能抑制异氟烷处理引起的VEGF分泌(P<0.01),但calphostin C对心肌细胞VEGF分泌无显著影响(P>0.05)。结论:异氟烷诱导心肌细胞释放VEGF,有可能是异氟烷心肌保护机制之一,蛋白激酶C参与异氟烷诱导的VEGF表达。

The Effect on the Expression of Vascular Endothelial Growth Factor Via Isoflurane in Cardiac Myocytes Algesia in Rats

Objective:To investigate the effect of isoflurane on Vascular endothelial growth factor(VEGF) expression and associated signaling pathway in cultured rat cardiac myocytes.Methods:Primary cultures of rat cardiomyocytes were randomized into the following groups:the control group:cells were incubated without any treatment;The isoflurane group:cells were treated with isoflurane at 0.5,1,1.5MAC respectivly for 6 hours; The PKC inhibitor group:cells were treated with PKC inhibitor calphostin C at a final concentration of 50nM;The PKC inhibitor + isoflurane group: cells were treated with 50nM calphostin C and IMAC isoflurane for 6 hours.VEGF expressions were identified by enzyme-linked immunosorbent assay.Results:Isoflurane dose dependently increased cardiac myocytes VEGF expression.The VEGF levels were significantly higher in 1MAC and 1,5MAC isoflurane group as compared with the control group(P<0.01).The effect of isoflurane on VEGF upregulation was blocked by PKC inhibitor calphostin C,however,calphostin did not alter VEGF expression(P>0.05).Conclusions:We demonstrated that isoflurane induced VEGF expression in cardiac myocytes through PKC,suggesting a possible novel mechanism of isoflurane induced cardiac protection.