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[目的]研究重组葡激酶(r-Sak)对大鼠重症急性胰腺炎(SAP)的发展及心肌损伤的干预作用,探讨其作用机制。[方法]63只SD大鼠随机分为假手术(A)组(n=9),模型对照(B)组(n=27),r-Sak治疗(C)组(n=27)。SAP模型采用5%牛磺胆酸钠胰胆管逆行注射方法建立。ELISA法测定6、12、18 h各时点血清肿瘤坏死因子α(TNF-α)、白细胞介素6(IL-6)、肌酸激酶同工酶(CK-MB)及心肌肌钙蛋白(CTn1)水平,免疫组化法检测术后6、121、8 h各时点心肌核转录因子-κB(NF-κB)的活化情况,光镜及电镜下观察胰腺及心肌组织的病理变化。[结果]大鼠从术后6 h开始出现CTn1、CK-MB升高,治疗组各时点较对照组明显下降(P<0.05)。IL-6、TNF-α水平亦从术后6 h开始升高,其变化在时点上与CTn1、CK-MB的变化具有一致性,治疗组各时点与对照组相比明显下降(P<0.05)。治疗组胰腺及心肌组织的出血坏死减轻,微血管血栓的形成减少。[结论]r-Sak能减轻SAP的病变程度和心肌损伤,可能具有治疗SAP及预防心肌损伤等并发症的作用,特异性溶栓剂的应用可能成为治疗SAP的新途径。
[Objective] To investigate the effect of recombinant staphylokinase (r-Sak) on the development of severe acute pancreatitis (SAP) and myocardial injury in rats and its mechanism of action. [Methods] Sixty - three SD rats were randomly divided into sham operation group (n = 9), model control group (n = 27) and r - Sak treatment group (n = 27). SAP model using 5% sodium taurocholate pancreaticobiliary retrograde injection method was established. Serum levels of tumor necrosis factor alpha (TNF-α), interleukin 6 (IL-6), creatine kinase MB (CK-MB) and cardiac troponin I CTn1 were detected by immunohistochemistry. The activation of nuclear factor-κB (NF-κB) was detected by immunohistochemistry at 6, 121 and 8 h after operation. Pathological changes of pancreas and myocardium were observed under light microscope and electron microscope. [Result] The levels of CTn1 and CK-MB in rats increased from 6 h after operation, and the levels of CTn1 and CK-MB in the treatment group were significantly lower than those in the control group at 6 h after operation (P <0.05). The levels of IL-6 and TNF-α also increased from 6 h after operation, and their changes were consistent with the changes of CTn1 and CK-MB at different time points. The levels of IL-6 and TNF- <0.05). Hemorrhagic necrosis of pancreas and myocardial tissue in the treatment group was reduced and the formation of microvascular thrombosis was reduced. [Conclusion] r-Sak can alleviate the severity of SAP and myocardial injury, may play a role in the treatment of SAP and prevention of complications such as myocardial injury. The application of specific thrombolytic agents may become a new way to treat SAP.