Caffeic Acid Phenethyl Ester Protects Kidney Mitochondria against Ischemia/Reperfusion Induced Injury in an In Vivo Rat Model.
Caffeic Acid Phenethyl Ester Protects Kidney Mitochondria against Ischemia/Reperfusion Induced Injury in an In Vivo Rat Model.
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咖啡酸苯乙酯在体内大鼠模型中保护肾脏线粒体免受缺血/再灌注诱导的损伤。
DOI：
10.3390/antiox10050747
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发表时间：
2021-05-08
期刊：
影响因子：
--
通讯作者：
Trumbeckaite S
中科院分区：
文献类型：
--
作者：
Kamarauskaite J;Baniene R;Trumbeckas D;Strazdauskas A;Trumbeckaite S
为了提高缺血/再灌流的耐受性，天然抗氧化剂受到了广泛的关注。咖啡酸苯乙酯(CAPE)是黑杨芽、幼叶和蜂胶的树脂性分泌物的活性成分，具有抗炎、抗氧化、免疫调节和心脏保护等独特的生物活性。缺乏研究表明CAPE的抗氧化潜力与CAPE在线粒体水平上的保护作用机制之间存在联系，线粒体是细胞基本功能的主要能量来源。在肾脏，缺血/再灌注损伤导致迅速的肾功能障碍和高死亡率，寻找具有生物活性的保护化合物仍然是非常现实的。因此，本研究的目的是确定CAPE的抗氧化能力，并探讨CAPE对在体大鼠肾脏缺血/再灌注损伤的保护作用。我们发现CAPE(1)具有抗氧化活性(CAPE的还原特性比其抗自由基特性更明显)；CAPE有效地降低细胞色素c；(2)保护谷氨酸/苹果酸氧化和复合体I的活性；(3)保护线粒体外膜免受损伤和细胞色素c的释放；(4)抑制复合体II(SDH)F位的活性氧(ROS)的产生；(5)减少缺血/再灌注诱导的LDH释放，防止细胞死亡；(6)对琥珀酸氧化和复合体II+III活性无保护作用，但对复合体II(SDH)的缺血再灌流损伤有部分保护作用。综上所述，我们的研究表明，咖啡酸苯乙酯在体内缺血/再灌注模型中保护肾脏线粒体氧化磷酸化，减少复合体II中ROS的产生，并显示出作为治疗药物开发抗氧化应激相关疾病的药物的潜力。
To improve ischemia/reperfusion tolerance, a lot of attention has been focused on natural antioxidants. Caffeic acid phenethyl ester (CAPE), an active component of the resinous exudates of the buds and young leaves of Populus nigra L., Baccharis sarothroides A., etc., and of propolis, possesses unique biological activities such as anti-inflammatory, antioxidant, immunomodulating, and cardioprotective effects, among others. There is a lack of studies showing a link between the antioxidant potential of CAPE and the mechanism of protective action of CAPE at the level of mitochondria, which produces the main energy for the basic functions of the cell. In the kidney, ischemia/reperfusion injury contributes to rapid kidney dysfunction and high mortality rates, and the search for biologically active protective compounds remains very actual. Therefore, the aim of this study was to identify the antioxidant potential of CAPE and to investigate whether CAPE can protect rat kidney mitochondria from in vivo kidney ischemia/reperfusion induced injury. We found that CAPE (1) possesses antioxidant activity (the reducing properties of CAPE are more pronounced than its antiradical properties); CAPE effectively reduces cytochrome c; (2) protects glutamate/malate oxidation and Complex I activity; (3) preserves the mitochondrial outer membrane from damage and from the release of cytochrome c; (4) inhibits reactive oxygen species (ROS) generation in the Complex II (SDH) F site; (5) diminishes ischemia/reperfusion-induced LDH release and protects from necrotic cell death; and (6) has no protective effects on succinate oxidation and on Complex II +III activity, but partially protects Complex II (SDH) from ischemia/reperfusion-induced damage. In summary, our study shows that caffeic acid phenethyl ester protects kidney mitochondrial oxidative phosphorylation and decreases ROS generation at Complex II in an in vivo ischemia/reperfusion model, and shows potential as a therapeutic agent for the development of pharmaceutical preparations against oxidative stress-related diseases.
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影响因子：
3.7
作者：
Chen Y;Xiao H;Zheng J;Liang G
通讯作者：
Liang G
DOI：
10.1016/b978-0-12-394309-5.00006-7
发表时间：
2012
影响因子：
--
作者：
Kalogeris, Theodore;Baines, Christopher P.;Krenz, Maike;Korthuis, Ronald J.
通讯作者：
Korthuis, Ronald J.
影响因子：
13.6
作者：
Jussupow, Alexander;Di Luca, Andrea;Kaila, Ville R., I
通讯作者：
Kaila, Ville R., I
影响因子：
7.4
作者：
Koleva, II;Niederländer, HAG;van Beek, TA
通讯作者：
van Beek, TA
影响因子：
4.8
作者：
Maklashina, Elena;Rajagukguk, Sany;Cecchini, Gary
通讯作者：
Cecchini, Gary