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Sufentanil protects the rat myocardium against ischemia–reperfusion injury via activation of the ERK1/2 pathway

机译：舒芬太尼通过激活ERK1 / 2途径保护大鼠心肌免受缺血再灌注损伤

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Sufentanil, a lipophilic opioid, is the most frequently used clinical drug for ischemic heart disease. The effects of sufentanil on MAPK signaling in ischemic heart disease were explored. The effects of sufentanil on ischemia–reperfusion (IR)-induced myocardial injury in a rat model were examined. The serum levels of CK, LDH, MDA and SOD, and the activities of Na+–K+-ATPase and Ca2+–Mg2+-ATPase were measured. The levels of total and phosphorylated ERK1/2, JNK, and p38 were measured by western blotting in the heart, and the myocardial H9C2 cell line was studied. Using the Cell Counting Kit-8, the growth rate of H9C2 cells affected by sufentanil was studied. The serum levels of CK, LDH and MDA were higher in the IR group than in the SO and SUF groups. The SOD level, as well as the activities of Na+–K+-ATPase and Ca2+–Mg2+-ATPase, were lower in the SO and SUF groups than in the IR group. The phosphorylated ERK1/2 level was lower in the IR group than in the SO and SUF groups. The growth rate of H9C2 cells increased with the concentration of sufentanil and the exposure time. The phosphorylated ERK level was upregulated by 4–12 h of sufentanil exposure, indicating that the effects were time-dependent. Furthermore, an inhibition of ERK signaling by chemical inhibition suppressed the sufentanil-mediated increase in the growth rate of H9C2 cells. Sufentanil appears to be beneficial for cases of worsening ischemic heart disease. Further studies are necessary before a clinical application is considered.
机译：舒芬太尼是一种亲脂性阿片类药物，是缺血性心脏病最常用的临床药物。探索了舒芬太尼对缺血性心脏病中MAPK信号传导的影响。研究了舒芬太尼对大鼠缺血再灌注（IR）引起的心肌损伤的影响。血清CK，LDH，MDA和SOD水平以及Na + –K + -ATPase和Ca 2 + –Mg的活性测定 2 + -ATPase。通过蛋白质印迹法测量心脏中总ERK1 / 2和磷酸化ERK1 / 2，JNK和p38的水平，并研究了心肌H9C2细胞系。使用细胞计数试剂盒8，研究了受舒芬太尼影响的H9C2细胞的生长速率。 IR组的血清CK，LDH和MDA水平高于SO和SUF组。 SOD水平以及Na + –K + -ATPase和Ca 2 + –Mg 2+ < SO和SUF组的/ sup--ATPase低于IR组。 IR组的磷酸化ERK1 / 2水平低于SO和SUF组。 H9C2细胞的生长速率随舒芬太尼浓度和暴露时间的增加而增加。舒芬太尼暴露4–12 h可使磷酸化ERK水平上调，表明其作用与时间有关。此外，通过化学抑制对ERK信号的抑制也抑制了舒芬太尼介导的H9C2细胞生长速率的增加。舒芬太尼似乎对缺血性心脏病恶化的病例有益。在考虑临床应用之前，需要进一步的研究。

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