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目的探讨脂多糖预处理对血管内皮生长因子(VEGF165)、促血管生成素1(Ang-1)与高迁移率族蛋白B1(HMGBx1)在缺血-再灌注损伤心肌中表达的影响。方法普通B6小鼠制作心肌缺血-再灌注动物模型,实验组手术前给予脂多糖。用TUNEL检测心肌细胞凋亡状况,用凝胶迁移率实验(EMSA)检测核转录因子(NF-κB)的活力,用Western blot检测VEGF165、Ang-1、HMGBx1在心肌中的表达。大鼠心肌成肌细胞H9c2,转染携带人VEGF165和Ang-1的腺病毒,随后过氧化氢刺激,检测HMGBx1的胞浆含量和NF-κB的活性。结果小剂量脂多糖预处理能显著促进VEGF165、Ang-1在缺血-再灌注损伤心肌中的早期表达,并同时显著减少HMGBx1的表达和抑制心肌细胞凋亡。细胞实验提示VEGF165和Ang-1联合使用能显著减少心肌细胞胞浆中HMGBx1的含量和NF-κB的活性。结论 VEGF165和Ang-1可能通过抑制NF-κB的活性,减少HMGBx1的含量而对心肌细胞产生直接保护作用。
Objective To investigate the effect of lipopolysaccharide preconditioning on the expression of vascular endothelial growth factor (VEGF165), angiopoietin 1 (Ang-1) and high mobility group box 1 protein (HMGBx1) in myocardium of ischemia-reperfusion injury. Methods Normal B6 mice were subjected to myocardial ischemia - reperfusion. The experimental group was given lipopolysaccharide before operation. The apoptosis of cardiomyocytes was detected by TUNEL. The nuclear translocation factor (NF-κB) activity was detected by EMSA. The expression of VEGF165, Ang-1 and HMGBx1 in myocardium was detected by Western blot. Myocardial myoblasts H9c2 were transfected with adenoviruses carrying human VEGF165 and Ang-1 followed by hydrogen peroxide stimulation to detect the cytoplasmic content of HMGBx1 and the activity of NF-κB. Results Low-dose lipopolysaccharide preconditioning could significantly promote the early expression of VEGF165 and Ang-1 in the myocardium of ischemia-reperfusion injury and significantly decrease the expression of HMGBx1 and inhibit cardiomyocyte apoptosis. Cell experiments suggest that VEGF165 and Ang-1 can significantly reduce the content of HMGBx1 and the activity of NF-κB in the cytoplasm of cardiomyocytes. Conclusion VEGF165 and Ang-1 may directly protect cardiomyocytes by inhibiting the activity of NF-κB and decreasing the content of HMGBx1.