scholarly journals Elevated Serum Potassium Concentration Alleviates Cerebral Ischemia-Reperfusion Injury via Mitochondrial Preservation

2018 ◽  
Vol 48 (4) ◽  
pp. 1664-1674 ◽  
Author(s):  
Nuo Li ◽  
Sina Qin ◽  
Lu Xie ◽  
Tao Qin ◽  
Yegui Yang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Cytochrome C ◽  
Cytochrome C Oxidase ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Elevated Serum ◽  
Cerebral Ischemia Reperfusion ◽  
Mptp Opening ◽  
Cerebral Ischemia Reperfusion Injury

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.

scholarly journals A Novel Neuroprotective Strategy for Ischemic Stroke: Transient Mild Acidosis Treatment by CO2 Inhalation at Reperfusion

2013 ◽  
Vol 34 (2) ◽  
pp. 275-283 ◽  
Author(s):  
Yan-Ying Fan ◽  
Zhe Shen ◽  
Ping He ◽  
Lei Jiang ◽  
Wei-wei Hou ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Ischemic Postconditioning ◽  
Cerebral Ischemia Reperfusion ◽  
Mptp Opening ◽  
Neuroprotective Strategy ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Cerebral Arterial Occlusion

Acidosis is one of the key components in cerebral ischemic postconditioning that has emerged recently as an endogenous strategy for neuroprotection. We set out to test whether acidosis treatment at reperfusion can protect against cerebral ischemia/reperfusion injury. Adult male C57BL/6 J mice were subjected to 60-minute middle cerebral arterial occlusion followed by 24-hour reperfusion. Acidosis treatment by inhaling 10%, 20%, or 30% CO2 for 5 or 10 minutes at 5, 50, or 100 minutes after reperfusion was applied. Our results showed that inhaling 20% CO2 for 5 minutes at 5 minutes after reperfusion-induced optimal neuroprotection, as revealed by reduced infarct volume. Attenuating brain acidosis with NaHCO3 significantly compromised the acidosis or ischemic postconditioning-induced neuroprotection. Consistently, both acidosis-treated primary cultured cortical neurons and acute corticostriatal slices were more resistant to oxygen–glucose deprivation/reperfusion insult. In addition, acidosis inhibited ischemia/reperfusion-induced apoptosis, caspase-3 expression, cytochrome c release to cytoplasm, and mitochondrial permeability transition pore (mPTP) opening. The neuroprotection of acidosis was inhibited by the mPTP opener atractyloside both in vivo and in vitro. Taken together, these findings indicate that transient mild acidosis treatment at reperfusion protects against cerebral ischemia/reperfusion injury. This neuroprotection is likely achieved, at least partly, by inhibiting mPTP opening and mitochondria-dependent apoptosis.

scholarly journals Underlying mechanisms of Electroacupuncture against Cerebral Ischemia-reperfusion Injury: Reduces Cell Apoptosisand Pyroptosis by Regulating Caspase-3 and Caspase-1

2021 ◽  
Author(s):  
Li Cai ◽  
Zeng-Yu Yao ◽  
Lu Yang ◽  
Xiu-Hong Xu ◽  
Meng Luo ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Knockout Mice ◽  
Caspase 3 ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Caspase 1 ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Abstract BackgroundCell apoptosis and pyroptosis are the primary forms of cerebral ischemia/reperfusion injury, and these two cell death methods are both regulated by the caspase gene family. Electroacupuncture can reduce the neuronal damage caused by cerebral ischemia/reperfusion. We hypothesized that inhibition of Caspase-1/Caspase-3 could be the mechanism of electroacupuncture against pyroptosis and apoptosis after cerebral ischemia/reperfusion injury. MethodsThe cerebral ischemia-reperfusion injury model of C57 and Caspase-1/Caspase-3 gene knockout mice was established by longa’ s method. Electroacupuncture was conducted at acupoints Chize (LU5), Hegu (LI4), Sanyinjiao (SP6), and Zusanli (ST36) 1.5 hours after ischemia/reperfusion injury for 20 minutes, and observation was carried out after 24h. Neurological deficit scores evaluated the neurological function, cerebral infarction volume was observed by TTC staining, neuronal apoptosis index was measured by TUNEL, and the protein expression of Caspase-1 and Caspase-3 was detected by Western blot assay. ResultsCompared with I/R group, EA group showed lower neurological deficit score, smaller cerebral infarction volume and lower degree of nerve cell injury (P<0.05). In EA group, the protein expression of Caspase-3 in C57 and caspase-1 knockout mice and Caspase-3 in C57 and caspase-3 knockout mice were lower than that in I/R group (P<0.05). ConclusionsElectroacupuncture plays a neuroprotective role by inhibiting the protein expression of Caspase-1 and Caspase-3, and reducing the activation of cell apoptosis and pyroptosis.

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