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小鼠心肌I/R模型中HIF-1α对IL-2的表达调控作用及其机制研究

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  • 中图分类号:

  • R541

摘要:

目的 探究小鼠心肌细胞的缺血/再灌注(I/R)模型中缺氧诱导因子-1α(HIF-1α)对白
细胞介素-2(IL-2)的表达调控作用和作用机制。方法 将60只小鼠随机分为对照组、I/R组、I/R+HIF-
1α组和I/R+siHIF-1α组四组(每组各15例)。采用经典结扎法构建I/R模型,尾静脉注射HIF-1α过表
达或siHIF-1α质粒(2 mg/kg)。注射等量阴性对照质粒作为对照。2周后检测各组小鼠的HIF-1α蛋
白、心肌损伤指标、心肌梗死面积、细胞凋亡、IL-2、VEGF mRNA和蛋白的水平。结果 四组小鼠的上
述指标比较,差异均有统计学意义(P<0.05)。I/R组的HIF-1α蛋白、肌酸激酶同工酶(CK-MB)、
肌钙蛋白T(cTnT)、心肌梗死面积、凋亡指数、IL-2和VEGF mRNA和蛋白的水平,显著高于对照组
(P<0.05)。I/R+HIF-1α组的HIF-1α蛋白、IL-2、VEGF mRNA和蛋白的水平显著高于I/R组,CKMB
、cTnT、梗死百分比、凋亡指数显著低于I/R组(P<0.05)。I/R+siHIF-1α组的HIF-1α蛋白、
IL-2、VEGF mRNA和蛋白的水平显著低于I/R组,CK-MB、cTnT、心肌梗死面积、凋亡指数显著高于I/R
组(P<0.05)。结论 小鼠心肌细胞的I/R模型中HIF-1α可通过促进IL-2的表达缓解心肌组织损伤。

Abstract:

Objective To investigate the regulation effect of hypoxia-inducible factor 1α (HIF-1α)
on interleukin-2 (IL-2) expression in mouse model of myocardial ischemia reperfusion (I/R), and study the
effective mechanism. Methods All mice (n=60) were divided into control group, I/R group, I/R+HIF-1α group
and I/R+siHIF-1α group (each n=15). The mouse model of myocardial I/R was established by applied classic
ligation. The overexpressed HIF-1α or siHIF-1α plasmids (2 mg/kg) were injected into mouse caudal vein. The
injection of negative control plasmid in equal amount was taken as control. The level of HIF-1α protein, indexes
of myocardial injury, infarction area, apoptosis, and level of interleukin-2 (IL-2) and mRNA and protein levels of
vascular endothelial growth factor (VEGF mRNA, VEGF protein) were detected in all groups after 2 weeks. Results
The differences in all above indexes had statistical significance among 4 groups (P<0.05). The levels of HIF-1α
protein, creatine kinase-MB isoenzyme (CK-MB) and cardiac troponin I (cTnI), infarction area, apoptosis index, and
levels of IL-2, VEGF mRNA and VEGF protein were significantly higher in I/R group than those in control group
(P<0.05). The levels of HIF-1α protein, IL-2, VEGF mRNA and VEGF protein were significantly higher, and CKMB,
cTnT, infarction percentage and apoptosis index were significantly lower in I/R+HIF-1α group than those in I/
R group (P<0.05). The levels of HIF-1α protein, IL-2, VEGF mRNA and VEGF protein were significantly lower,
and CK-MB, cTnT, infarction area and apoptosis index were significantly higher I/R+siHIF-1α group than those
in I/R group (P<0.05). Conclusion HIF-1α can relieve myocardial injury through improving IL-2 expression in
mouse model of myocardial I/R.

基金项目:

湖北省教育厅科学技术研究计划指导性项目
(B2018001)

参考文献:

  • 2008

  • 1

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