首页|PGC-1α参与心脏骤停复苏后心脏的保护及其作用机制

PGC-1α参与心脏骤停复苏后心脏的保护及其作用机制

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目的 探讨心脏骤停复苏后线粒体通过过氧化物酶体增殖物激活受体γ共激活因子-1α(PGC-1α)参与对心脏的保护作用及机制.方法 将18只雄性SD大鼠采用信封法分为对照组、PGC-1α组,记录实验前基础生命体征;通过窒息法构建大鼠心脏骤停模型,复苏成功后,给予对照组股静脉注射0.9%氯化钠注射液,PGC-1α组股静脉注射PGC-1α激活剂(22 g/L),均0.25 mL/只.24 h后处死大鼠,抽取主动脉血,解剖剥离心脏.HE染色观察心肌病理损伤情况,检测并比较复苏30 min后及24 h后动脉血肌钙蛋白T(cTnT)、复苏24 h后的血气指标[pH、PCO2、PO2、剩余碱(BE)]和心脏组织ATP含量;ELISA法检测血清中IL-6、TNF-α表达水平,qRT-PCR法检测心脏组织IL-6、TNF-α mRNA相对表达量.结果 大鼠心脏骤停复苏后24 h,对照组心肌结构破坏,肌纤维断裂,出现大量空泡细胞.相比对照组,复苏成功30 min后,PGC-1α组cTnT无明显变化;复苏24 h后,PGC-1α组cTnT含量显著降低,pH值显著升高,PCO2显著降低,PO2显著升高,BE显著升高,ATP含量显著升高,差异均有统计学意义(均P<0.05).复苏成功24 h后,PGC-1α组血清IL-6、TNF-α表达水平及心脏组织中TNF-α、IL-6 mRNA相对表达量均显著下降,差异均有统计学意义(均P<0.05).结论 心脏骤停复苏后,心脏出现再灌注损伤,线粒体通过PGC-1 α参与对心脏的保护作用.
Cardioprotective effect of PGC-1α in cardiac arrest rats after resuscitation
Objective To investigating the cardioprotective effect of peroxisome proliferator activated receptor γ coactivator-1α(PGC-1α)in cardiac arrest rats after resuscitation.Methods Eighteen male SD rats were randomly divided into a control group and a PGC-1α group.Cardiac arrest model was induced by asphyxia in rats and basic vital signs were recorded before modelling.After successful resuscitation,the control group received 0.9%normal saline chloride injection,while the PGC-1α group received PGC-1α activator(22 g/L),both 0.25 mL for each rats;24 h later the rats were sacrificed and heart samples were harvisted for pathology examination.Cardiac troponin T(cTnT)levels were measured 30 min and 24 h after resuscitation.Blood gas analysis[pH,PCO2,PO2,base excess(BE)]was performed,and ATP content in the heart was measured with ATP test kit at the 24 h following resuscitation.Serum levels of IL-6 and TNF-α were measured by ELISA and the relative expression levels of IL-6 and TNF-α mRNA in cardiac tissure were detected by qRT-PCR.Results The myocardium in the control group showed signs of destruction,with broken muscle fibers and a significant increase in vacuolar cells 24 h after resuscitation.Compared to the control group,there was no signifant change of cTnT after 30 min of resuscitation;and 24 h after resuscitation,the PGC-1α group exhibited a significant decrease of cTnT content and PCO2,a increase of pH,PO2,BE and ATP content(all P<0.05).Furthermore,serum levels of IL-6 and TNF-α were significantly decreased in the PGC-1α group compared to the control group;the relative expression levels of TNF-α and IL-6 mRNA in heart tissue were also significantly decreased(all P<0.05).Conclusion The study indicates that mitoc-hondria may play a protective role in cardiac reperfusion injury due to cardiac arrest through PGC-1α signaling pathway in rats.

Cardiac arrestResuscitationMitochondriaPeroxisome proliferator activated receptor γ coactivator-1αIschemia reperfusion

胡海燕、宋心玥、王利分、许媚、刘刚

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310021 杭州市急救中心科教培训科

温州医科大学附属第二医院呼吸科

310021 杭州市急救中心急救科

心脏骤停 复苏 线粒体 过氧化物酶体增殖物激活受体γ共激活因子-1α 缺血再灌注

浙江省医药卫生科技计划项目杭州市科技局项目

2024KY1420A20220325

2024

浙江医学
浙江省医学会

浙江医学

CSTPCD
影响因子:0.428
ISSN:1006-2785
年,卷(期):2024.46(19)