[1]刘祥,景桂霞,白娟,等.舒芬太尼预处理对大鼠心肌缺血再灌注时PI3K/Akt的影响[J].南方医科大学学报,2014,(03):335.
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舒芬太尼预处理对大鼠心肌缺血再灌注时PI3K/Akt的影响()
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《南方医科大学学报》[ISSN:/CN:]

卷:
期数:
2014年03期
页码:
335
栏目:
出版日期:
2014-03-15

文章信息/Info

Title:
Effect of sufentanil preconditioning on myocardial P-Akt expression in rats during
myocardial ischemia-reperfusion
作者:
刘祥景桂霞白娟袁慧
关键词:
舒芬太尼预处理心肌缺血再灌注损伤PI3K/Akt信号通路
Keywords:
sufentanil preconditioning PI3K/Akt signaling pathway ischemia/reperfusion injury
摘要:
目的研究舒芬太尼预处理对大鼠心肌缺血再灌注损伤的影响及PI3K/Akt(P-Akt)信号通路在其中的作用。方法选择健
康雄性大鼠60只,体质量250~350 g,随机分为5组:假手术组(Sham组),缺血再灌注组(I/R组),舒芬太尼预处理组(Spc组),舒
芬太尼预处理联合PI3K抑制剂组(Spc+W组),PI3K抑制剂组(W组)。通过结扎大鼠左冠状动脉前降支30 min,松开结扎
线复灌120 min制作心肌缺血再灌注模型。Sham组:只挂线,不结扎,持续150 min;I/R组:缺血30 min,再灌注120 min;Spc组:
缺血前采用微量注射泵股静脉泵注舒芬太尼1 μg/kg,泵注5 min,停止5 min,重复处理3次,总量共3 μg/kg的预处理方式,缺血
30 min,再灌注120 min;Spc+Wortmannin 组:舒芬太尼预处理前5 min给予PI3K抑制剂(15 μg/kg),缺血前30 min舒芬太尼预
处理,缺血30 min,再灌注120 min;Wortmannin 组:缺血前35 min给予PI3K抑制剂(15 μg/kg),缺血30 min,再灌注120 min。
于基础状态(T0)、缺血前即刻(T1)、缺血30 min(T2)、再灌注30 min(T3)、再灌注120 min(T4)记录各组大鼠心率和平均动脉压。
再灌注末抽取动脉血,离心取血清测定肌酸激酶同工酶(CK-MB)和乳酸脱氢酶(LDH)。实验结束时,各组取6只大鼠心脏测算
心肌梗死面积,其余6只大鼠采用Western blot测定心肌组织P-Akt的表达。结果与Sham组比较,I/R 组和Spc组P-Akt表达增
高(P<0.01),Spc+W组和W组P-Akt表达水平差异无统计学意义(P>0.05)。与I/R 组相比,Spc组心肌梗死面积减少(P<0.01),
CK-MB(P<0.01)、LDH(P<0.01)降低,心肌组织P-Akt 表达上调(P<0.01),平均动脉压略有上升,但无统计学差异(P>0.05),
Spc+W组和W组梗死面积、CK-MB、LDH差异无统计意义(P>0.05)。结论舒芬太尼预处理可减轻大鼠心肌缺血再灌注损伤,
增加P-Akt的表达,这种保护作用可能与PI3K/Akt信号通路的激活有关。
Abstract:
Objective To study the protective effect of sufentanil preconditioning against myocardial ischemia-reperfusion (I/R)
injury and the role of PI3K/Akt signaling pathway. Methods Sixty male SD rats weighing 250-350 g were randomly divided
into 5 equal groups, namely the sham-operated group, I/R group, sufentanil preconditioning group (Spc group), sufentanil
preconditioning + PI3K inhibitor group (Spc +W group), and PI3K inhibitor group (W group). Myocardial I/R model was
established by ligation of the anterior descending branch of the left coronary artery for 30 min followed by reperfusion for 120
min. Sufentanil was administered in 3 doses via the femoral vein before the occlusion, each at 1 μg/kg infused within 5 min at
a 5-min interval. In Spc +W and W groups, PI3K inhibitor wortmannin (15 μg/kg) was given intravenously 5 min before
sufentanil preconditioning and 35 min before ischemia, respectively. Heart rate and mean arterial pressure (MAP) were
continuously monitored during I/R. At the end of reperfusion, blood samples were obtained to determine plasma activation of
CK-MB and LDH. Acute infarct size was measured by triphenyltetrazolium chloride staining, and the myocardial tissues were
obtained to detect the expression of phosphorylated Akt using Western blotting. Results Phosphorylated Akt expression was
significantly up-regulated in I/R and Spc groups as compared with the sham group, and was significantly higher in Spc group
than in I/R group. After reperfusion, sufentanil preconditioning significantly decreased myocardial infarct size (P<0.01) and
lowered the levels of CK-MB (P<0.01) and LDH (P<0.01) compared with those in the I/R group. The I/R , Spc+W and W groups
showed no significant differences in myocardial infarct size or the levels of CK-MB and LDH. Conclusion The protective effect
of sufentanil preconditioning against myocardium against I/R injury in rats may involve PI3K/Akt signaling pathway
activation.

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更新日期/Last Update: 1900-01-01