PER2 Regulates Reactive Oxygen Species Production in the Circadian Susceptibility to Ischemia/Reperfusion Injury in the Heart.
PER2 Regulates Reactive Oxygen Species Production in the Circadian Susceptibility to Ischemia/Reperfusion Injury in the Heart.
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PER2 调节活性氧的产生，从而影响心脏缺血/再灌注损伤的昼夜节律易感性
DOI：
10.1155/2021/6256399
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发表时间：
2021
影响因子：
--
通讯作者：
Li L
中科院分区：
文献类型：
--
作者：
Weng Y;Li H;Gao L;Guo W;Xu S;Li L
本研究的主要目的是研究心肌缺血-再灌注（I/R）损伤中第2阶段（PER 2）表达的昼夜差异。我们研究了体外和体内心肌I/R后氧化应激和能量代谢的昼夜变化。此外，我们还分析了H2 O2处理和血清休克对转染针对Per 2的沉默RNA（siRNA-Per 2）的H9 c2细胞的影响。本研究以C57 BL/6雄性小鼠为研究对象，采用同步化昼夜节律的方法，分别在ZT 2和ZT 14建立了大鼠心肌缺血再灌注损伤模型。我们的体内分析表明，心肌梗死引起的损伤严重程度存在昼夜差异，白天发生的损伤更多。PER 2在心脏组织中白天显著降低，夜间较高。我们的研究结果还表明，在白天线粒体功能损伤越严重，产生更多的活性氧（ROS）和减少ATP，这增加了心肌损伤。在体外，我们的研究结果呈现出类似的趋势，表明当PER 2表达较低时，H9 c2细胞的凋亡增加。同时，下调PER 2通过增加ROS和线粒体损伤破坏氧化平衡。结果是ATP减少，无法为心肌细胞提供足够的能量保护。
The main objective of this study was to investigate the diurnal differences in Period 2 (PER2) expression in myocardial ischemia-reperfusion (I/R) injury. We investigated diurnal variations in oxidative stress and energy metabolism after myocardial I/R in vitro and in vivo. In addition, we also analyzed the effects of H2O2 treatment and serum shock in H9c2 cells transfected with silencing RNA against Per2 (siRNA-Per2) in vitro. We used C57BL/6 male mice to construct a model of I/R injury at zeitgeber time (ZT) 2 and ZT14 by synchronizing the circadian rhythms. Our in vivo analysis demonstrated that there were diurnal differences in the severity of injury caused by myocardial infarctions, with more injury occurring in the daytime. PER2 was significantly reduced in heart tissue in the daytime and was higher at night. Our results also showed that more severe injury of mitochondrial function in daytime produced more reactive oxygen species (ROS) and less ATP, which increased myocardial injury. In vitro, our findings presented a similar trend showing that apoptosis of H9c2 cells was increased when PER2 expression was lower. Meanwhile, downregulation of PER2 disrupted the oxidative balance by increasing ROS and mitochondrial injury. The result was a reduction in ATP and failure to provide sufficient energy protection for cardiomyocytes.
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影响因子：
3.7
作者：
Bartman CM;Oyama Y;Brodsky K;Khailova L;Walker L;Koeppen M;Eckle T
通讯作者：
Eckle T
影响因子：
82.9
作者：
通讯作者：
--
影响因子：
20.1
作者：
Durgan DJ;Pulinilkunnil T;Villegas-Montoya C;Garvey ME;Frangogiannis NG;Michael LH;Chow CW;Dyck JR;Young ME
通讯作者：
Young ME
DOI：
10.1152/ajpheart.00472.2006
发表时间：
2006-11-01
影响因子：
4.8
作者：
Eckle, Tobias;Grenz, Almut;Eltzschig, Holger K.
通讯作者：
Eltzschig, Holger K.
影响因子：
64.5
作者：
Balsalobre, A;Damiola, F;Schibler, U
通讯作者：
Schibler, U