Polydatin – a new mitochondria protector for acute severe hemorrhagic shock treatment
Polydatin – a new mitochondria protector for acute severe hemorrhagic shock treatment
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DOI：
10.1517/13543784.2013.748033
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发表时间：
2013-01
影响因子：
6.1
通讯作者：
Xingmin Wang;R. Song;Yun-yan Chen;Ming Zhao;K. Zhao
中科院分区：
文献类型：
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作者：
Xingmin Wang;R. Song;Yun-yan Chen;Ming Zhao;K. Zhao
目的：本研究的目的是了解严重休克时是否存在神经元线粒体损伤，并探索治疗严重休克的有效方法。研究设计和方法：将大鼠分为假手术组、休克+生理盐水组、休克+环孢素A组、休克+白藜芦醇组和休克+虎杖苷组。大鼠休克2 h后，给予生理盐水、环孢霉素A（CsA）、地塞米松（Res）和顺铂（PD），并输注失血。测定线粒体的形态、代谢和功能。结果如下：休克+ NS组神经元脂质过氧化物（LPO）水平升高，溶酶体损伤，线粒体通透性转换孔开放，线粒体肿胀，嵴模糊，线粒体膜电位（Δ E）降低，ATP含量减少，提示线粒体功能障碍。应用CsA、Res和PD等线粒体保护剂可部分抑制上述变化，尤其是PD保护后，ATP含量由休克+ NS组的44.14 ± 13.81%增加到89.57 ± 9.21%，存活时间由休克+ NS组的6.3 ± 5.9 h延长到休克+ PD组的31.6 ± 13.7 h。结论：本研究表明，神经元线粒体损伤参与了严重休克的发生，PD可能是严重休克时保护神经元线粒体损伤的最佳选择。
Objective: The aim of the study was find out whether neuronal mitochondrial injury does take place in severe shock and to explore effective therapy for severe shock. Research design and methods: Rats were divided in the following group: sham, shock + normal saline (NS), shock + cyclosporine A (CsA), shock + resveratrol (Res) and shock + polydatin (PD). Rats were subjected to shock for 2 h, followed by administration of NS, CsA, Res and PD, and infusion of shed blood. Morphology, metabolism and function of mitochondria were measured. Results: Increased lipid peroxides (LPO) levels, lysosomal injury and mitochondrial permeability transition pore opening took place in neurons, resulting in swollen mitochondria with poorly defined cristae, decreased mitochondrial membrane potential (ΔΨ) and reduced ATP content in shock + NS group, indicating mitochondrial dysfunction. Mitochondrial protectors, such as CsA, Res and PD, partially inhibited these alterations, especially following PD protection, ATP level increased from 44.14 ± 13.81% in shock + NS group to 89.57 ± 9.21% and the survival time was prolonged from 6.3 ± 5.9 h in the shock + NS group to 31.6 ± 13.7 h in shock + PD group. Conclusions: The study shows that neuronal mitochondrial injury is involved in the genesis of severe shock and PD may be the best choice for protection of neuron against mitochondrial injury in severe shock.