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首页> 外文期刊>Cellular Physiology and Biochemistry >Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation
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Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation

机译：血清钾浓度升高通过线粒体保存减轻了脑缺血-再灌注损伤

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Background/Aims The anti-apoptotic effect of an increase in the extracellular concentration of potassium ([K+]) has been confirmed in vitro. However, it is not yet known whether elevated serum [K+] exerts a cerebroprotective effect in vivo. In this study, we aimed to explore the effect of elevated serum [K+] in a rat model of middle cerebral artery occlusion and reperfusion (MCAO/R). Methods Rats subjected to 90-min MCAO received 2.5% KCL, 1.25% KCL, or a normal saline solution at a dose of 3.2 mL/kg at the onset of reperfusion. Rats that were subjected to vascular exposure and ligation without MCAO were defined as the Sham group. Serum [K+] was determined using a blood gas analyzer at 1 min after medicine administration. At 24 h post-reperfusion, rat brains were harvested and processed for 2% 2,3,5-triphenyltetrazolium chloride staining, terminal deoxynucleotidyl transferase-mediated 2′-deoxyuridine 5′-triphosphate-biotin nick end labeling staining, detection of caspase-3 and cleaved-caspase-3 by western blotting, detection of reactive oxygen species (ROS) by dihydroethidium staining, and observation of mitochondrial structure by electron microscopy. In addition, malondialdehyde (MDA), adenosine triphosphate (ATP), total superoxide dismutase (T-SOD), cytochrome C oxidase (COX) activity, and mitochondrial permeability transition pore (MPTP) opening were measured using detection kits. Results The results showed that elevated serum [K+] decreased cerebral injury and apoptosis, reduced ROS and MDA levels and MPTP opening, increased ATP levels and cytochrome C oxidase activity, and improved mitochondrial ultrastructural changes, although there was no significant difference in T-SOD activity. Conclusion These findings suggested that elevated serum [K+] could alleviate cerebral ischemia-reperfusion injury and the mechanism may be associated with the preservation of mitochondrial function.
机译：背景/目的已在体外证实了增加细胞外钾浓度（[K +]）的抗凋亡作用。然而，尚不清楚升高的血清[K +]是否在体内发挥了脑保护作用。在这项研究中，我们旨在探讨升高的血清[K +]在大脑中动脉闭塞和再灌注（MCAO / R）大鼠模型中的作用。方法在再灌注开始时，接受90分钟MCAO的大鼠接受2.5％KCL，1.25％KCL或3.2 mL / kg的生理盐水。将未进行MCAO的血管暴露和结扎的大鼠定义为假手术组。给药后1分钟，使用血气分析仪测定血清[K +]。再灌注后24小时，收集大鼠大脑并进行2％2,3,5-三苯基四唑氯化物染色，末端脱氧核苷酸转移酶介导的2'-脱氧尿苷5'-三磷酸-生物素缺口末端标记染色，caspase-通过蛋白质印迹法检测3和裂解的caspase-3，通过二氢乙啶染色检测活性氧（ROS），并通过电子显微镜观察线粒体结构。此外，使用检测试剂盒测量了丙二醛（MDA），三磷酸腺苷（ATP），总超氧化物歧化酶（T-SOD），细胞色素C氧化酶（COX）活性和线粒体通透性转换孔（MPTP）的开口。结果结果表明，升高的血清[K +]减少了脑损伤和细胞凋亡，降低了ROS和MDA水平和MPTP的开放，增加了ATP水平和细胞色素C氧化酶的活性，并改善了线粒体的超微结构变化，尽管T-SOD没有显着差异活动。结论这些发现提示血清[K +]升高可减轻脑缺血再灌注损伤，其机制可能与维持线粒体功能有关。

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