Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro.
Potential Effects of Poloxamer 188 on Rat Isolated Brain Mitochondria after Oxidative Stress In Vivo and In Vitro.
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DOI：
10.3390/brainsci11010122
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发表时间：
2021-01-18
期刊：
影响因子：
3.3
通讯作者：
Riess ML
中科院分区：
文献类型：
--
作者：
Pille JA;Riess ML
脑缺血后的结果往往是令人沮丧的。再灌注显著增加了缺血性损伤本身。因此，迫切需要针对缺血/再灌注（I/R）损伤的新策略。泊洛沙姆（P）188是一种两亲性三嵌段共聚物，是一种非常有前途的药理学治疗剂，因为其插入损伤细胞膜的能力已被报道在各种模型中保护免受I/R损伤。虽然线粒体功能特别受益于I/R后P188治疗，但仍不清楚这种有益作用是直接还是间接发生的。在这里，大鼠分离的脑线粒体进行氧化应激在体内窒息心脏骤停或在体外通过添加过氧化氢（H2 O2）分离后。线粒体功能通过三磷酸腺苷合成、耗氧量和钙潴留能力进行评估。窒息和H2 O2暴露显著损害线粒体功能。P188在任一损伤机制后均不保留线粒体功能。进一步的研究表明。
Outcome after cerebral ischemia is often dismal. Reperfusion adds significantly to the ischemic injury itself. Therefore, new strategies targeting ischemia/reperfusion (I/R) injury are critically needed. Poloxamer (P)188, an amphiphilic triblock copolymer, is a highly promising pharmacological therapeutic as its capability to insert into injured cell membranes has been reported to protect against I/R injury in various models. Although mitochondrial function particularly profits from P188 treatment after I/R, it remains unclear if this beneficial effect occurs directly or indirectly. Here, rat isolated brain mitochondria underwent oxidative stress in vivo by asphyxial cardiac arrest or in vitro by the addition of hydrogen peroxide (H2O2) after isolation. Mitochondrial function was assessed by adenosine triphosphate synthesis, oxygen consumption, and calcium retention capacity. Both asphyxia and H2O2 exposure significantly impaired mitochondrial function. P188 did not preserve mitochondrial function after either injury mechanism. Further research is indicated.
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影响因子：
9.5
作者：
Baines CP
通讯作者：
Baines CP
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.
DOI：
10.1073/pnas.052713199
发表时间：
2002-03-05
影响因子：
11.1
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通讯作者：
Weiss, JN
影响因子：
5.5
作者：
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通讯作者：
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影响因子：
6.3
作者：
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通讯作者：
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