Short-term dietary restriction ameliorates brain injury after cardiac arrest by modulation of mitochondrial biogenesis and energy metabolism in rats.
Short-term dietary restriction ameliorates brain injury after cardiac arrest by modulation of mitochondrial biogenesis and energy metabolism in rats.
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短期饮食限制可通过调节大鼠的线粒体生物发生和能量代谢来缓解心脏骤停后的脑损伤。
DOI：
10.21037/atm-20-3075
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发表时间：
2021-01
影响因子：
--
通讯作者：
Wang P
中科院分区：
文献类型：
--
作者：
Zhou M;Yu T;Fang X;Ge Q;Song F;Huang Z;Jiang L;Wang P
饮食限制（DR）是一种众所周知的干预措施，可延长寿命并抵抗多种形式的急性应激，包括缺血再灌注损伤。然而，DR对心脏骤停（CA）后神经损伤的影响仍不清楚。使用窒息CA模型在大鼠中研究短期DR（每日饮食减少70%一周）对神经损伤的影响。使用Kaplan-Meier生存分析获得生存曲线。采用酶联免疫吸附法检测血清S-100β水平。用末端脱氧核糖核苷酸转移酶dUTP缺口末端标记法和尼氏染色法检测细胞凋亡和神经元损伤。采用8-羟基脱氧鸟苷（8-OHdG）免疫组化染色评价氧化应激。线粒体的生物合成进行了检查，通过电子显微镜和线粒体DNA拷贝数测定。Western blot检测蛋白表达。活性氧（ROS）和代谢产物水平通过相应的检测试剂盒进行测定。短期DR可显著改善CA后3天生存率、神经功能缺损评分（NDS）和降低血清S-100β水平。短期DR还显著减弱CA后脑中的细胞凋亡、神经元损伤和氧化应激。此外，短期DR增加CA后线粒体生物合成以及脑PGC-1α和SIRT 1蛋白表达。此外，短期DR增加了三磷酸腺苷、β-羟基丁酸、乙酰辅酶A水平和烟酰胺腺嘌呤二核苷酸（NAD+）/还原型NAD+（NADH）比值，并降低了血清乳酸水平。氧化应激的减少、线粒体生物合成的上调和酮体代谢的增加可能在短期DR下CA后神经功能的保护中起关键作用。
Dietary restriction (DR) is a well-known intervention that increases lifespan and resistance to multiple forms of acute stress, including ischemia reperfusion injury. However, the effect of DR on neurological injury after cardiac arrest (CA) remains unknown. The effect of short-term DR (one week of 70% reduced daily diet) on neurological injury was investigated in rats using an asphyxial CA model. The survival curve was obtained using Kaplan-Meier survival analysis. Serum S-100β levels were detected by enzyme linked immunosorbent assay. Cellular apoptosis and neuronal damage were assessed by terminal deoxyribonucleotide transferase dUTP nick end labeling assay and Nissl staining. The oxidative stress was evaluated by immunohistochemical staining of 8-hydroxy-2'-deoxyguanosine (8-OHdG). Mitochondrial biogenesis was examined by electron microscopy and mitochondrial DNA copy number determination. The protein expression was detected by western blot. The reactive oxygen species (ROS) and metabolite levels were measured by corresponding test kits. Short-term DR significantly improved 3-day survival, neurologic deficit scores (NDS) and decreased serum S-100β levels after CA. Short-term DR also significantly attenuated cellular apoptosis, neuronal damage and oxidative stress in the brain after CA. In addition, short-term DR increased mitochondrial biogenesis as well as brain PGC-1α and SIRT1 protein expression after CA. Moreover, short-term DR increased adenosine triphosphate, β-hydroxybutyrate, acetyl-CoA levels and nicotinamide adenine dinucleotide (NAD+)/reduced form of NAD+ (NADH) ratios as well as decreased serum lactate levels. Reduction of oxidative stress, upregulation of mitochondrial biogenesis and increase of ketone body metabolism may play a crucial role in preserving neuronal function after CA under short-term DR.
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DOI：
10.1016/j.bbadis.2013.09.007
发表时间：
2014-08
影响因子：
6.2
作者：
Jin, Huajun;Kanthasamy, Arthi;Ghosh, Anamitra;Anantharam, Vellareddy;Kalyanaraman, Balaraman;Kanthasamy, Anumantha G.
通讯作者：
Kanthasamy, Anumantha G.
影响因子：
5.4
作者：
Kilbaugh TJ;Sutton RM;Karlsson M;Hansson MJ;Naim MY;Morgan RW;Bratinov G;Lampe JW;Nadkarni VM;Becker LB;Margulies SS;Berg RA
通讯作者：
Berg RA
影响因子：
7.1
作者：
Fernandez-Marcos, Pablo J.;Auwerx, Johan
通讯作者：
Auwerx, Johan
影响因子：
6.5
作者：
Donnino, Michael W.;Liu, Xiaowen;Callaway, Clifton W.
通讯作者：
Callaway, Clifton W.
影响因子：
6.3
作者：
Chowdhury, Golam M. I.;Jiang, Lihong;Behar, Kevin L.
通讯作者：
Behar, Kevin L.