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目的研究缺血预适应(ischemicpreconditioning,IPC)和缬沙坦(valsartan)在缺血/再灌注(I/R)损伤时与信号转导及转录激活因子3(STAT3)的关系,及其对心脏的保护作用。方法将32只Wistar大鼠随机分为4组(每组8只),分别为I/R组、IPC组、缬沙坦I/R(VIR)组、和缬沙坦IPC(VIPC)组,I/R组和IPC组合称为生理盐水组,VIR组和VIPC组合称为缬沙坦组。用ELISA方法检测血清IL-6的水平,并留取梗死区心肌组织用免疫组化染色法,检测STAT3的磷酸化。结果IPC组与I/R组相比,STAT3的磷酸化明显增加(P<0.01),IL-6的水平降低(P<0.01)。缬沙坦组与生理盐水组相比,STAT3的磷酸化和血清IL-6的水平明显降低(P<0.01)。结论IPC通过STAT3磷酸化,可激活心肌存活通路,抑制炎症因子的表达,减轻I/R损伤。缬沙坦可部分抑制STAT3活化,抑制IL-6的表达,并产生心脏保护作用。
Objective To investigate the relationship between ischemic preconditioning (IPC) and valsartan on signal transducers and activators of transcription 3 (STAT3) during ischemia / reperfusion (I / R) injury and its effect on heart The protective effect. Methods Thirty-two Wistar rats were randomly divided into 4 groups (8 in each group): I / R group, IPC group, Valsartan I / R (VIR) group and Valsartan IPC (VIPC) I / R group and IPC combination is called saline group, VIR group and VIPC combination is called valsartan group. Serum levels of IL-6 were detected by ELISA, myocardial infarction area was taken for immunohistochemical staining to detect the phosphorylation of STAT3. Results Compared with I / R group, the phosphorylation of STAT3 increased significantly (P <0.01) and the level of IL-6 decreased (P <0.01). Compared with the saline group, the phosphorylation of STAT3 and the level of serum IL-6 in the valsartan group were significantly decreased (P <0.01). Conclusion IPC phosphorylation by STAT3 can activate myocardial viability pathway, inhibit the expression of inflammatory cytokines and reduce I / R injury. Valsartan can partially inhibit STAT3 activation, inhibit IL-6 expression and produce cardioprotection.