Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation
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...
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Cell Physiol Biochem Press GmbH & Co KG
2018-08-01
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Online Access: | https://www.karger.com/Article/FullText/492289 |
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author | Nuo Li Sina Qin Lu Xie Tao Qin Yegui Yang Wei Fang Meng-hua Chen |
author_facet | Nuo Li Sina Qin Lu Xie Tao Qin Yegui Yang Wei Fang Meng-hua Chen |
author_sort | Nuo Li |
collection | DOAJ |
description | 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. |
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spelling | doaj.art-df43ffab9e77483b831a51274fe65c2a2022-12-21T19:20:46ZengCell Physiol Biochem Press GmbH & Co KGCellular Physiology and Biochemistry1015-89871421-97782018-08-014841664167410.1159/000492289492289Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial PreservationNuo LiSina QinLu XieTao QinYegui YangWei FangMeng-hua ChenBackground/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.https://www.karger.com/Article/FullText/492289KclIschemia-reperfusion injuryMitochondriaApoptosis |
spellingShingle | Nuo Li Sina Qin Lu Xie Tao Qin Yegui Yang Wei Fang Meng-hua Chen Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation Cellular Physiology and Biochemistry Kcl Ischemia-reperfusion injury Mitochondria Apoptosis |
title | Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation |
title_full | Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation |
title_fullStr | Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation |
title_full_unstemmed | Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation |
title_short | Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation |
title_sort | elevated serum potassium concentration alleviates cerebral ischemia reperfusion injury via mitochondrial preservation |
topic | Kcl Ischemia-reperfusion injury Mitochondria Apoptosis |
url | https://www.karger.com/Article/FullText/492289 |
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