scholarly journals Free Radical Damage in Ischemia-Reperfusion Injury: An Obstacle in Acute Ischemic Stroke after Revascularization Therapy

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Ming-Shuo Sun ◽  
Hang Jin ◽  
Xin Sun ◽  
Shuo Huang ◽  
Fu-Liang Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Free Radical ◽  
Acute Ischemic Stroke ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Free Radical Damage ◽  
Revascularization Therapy ◽  
Radical Damage ◽  
Neuroprotective Therapies

Acute ischemic stroke is a common cause of morbidity and mortality worldwide. Thrombolysis with recombinant tissue plasminogen activator and endovascular thrombectomy are the main revascularization therapies for acute ischemic stroke. However, ischemia-reperfusion injury after revascularization therapy can result in worsening outcomes. Among all possible pathological mechanisms of ischemia-reperfusion injury, free radical damage (mainly oxidative/nitrosative stress injury) has been found to play a key role in the process. Free radicals lead to protein dysfunction, DNA damage, and lipid peroxidation, resulting in cell death. Additionally, free radical damage has a strong connection with inducing hemorrhagic transformation and cerebral edema, which are the major complications of revascularization therapy, and mainly influencing neurological outcomes due to the disruption of the blood-brain barrier. In order to get a better clinical prognosis, more and more studies focus on the pharmaceutical and nonpharmaceutical neuroprotective therapies against free radical damage. This review discusses the pathological mechanisms of free radicals in ischemia-reperfusion injury and adjunctive neuroprotective therapies combined with revascularization therapy against free radical damage.

scholarly journals Somatosensory Cortical Electrical Stimulation After Reperfusion Attenuates Ischemia/Reperfusion Injury of Rat Brain

2021 ◽  
Vol 13 ◽  
Author(s):  
Liang-Chao Wang ◽  
Wei-Yen Wei ◽  
Pei-Chuan Ho ◽  
Pei-Yi Wu ◽  
Yuan-Ping Chu ◽  
...  
Keyword(s):  
Electrical Stimulation ◽  
Ischemic Stroke ◽  
Adjuvant Therapy ◽  
Acute Ischemic Stroke ◽  
Reperfusion Injury ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Therapeutic Window

Objective: Ischemic stroke is an important cause of death and disability worldwide. Early reperfusion by thrombolysis or thrombectomy has improved the outcome of acute ischemic stroke. However, the therapeutic window for reperfusion therapy is narrow, and adjuvant therapy for neuroprotection is demanded. Electrical stimulation (ES) has been reported to be neuroprotective in many neurological diseases. In this study, the neuroprotective effect of early somatosensory cortical ES in the acute stage of ischemia/reperfusion injury was evaluated.Methods: In this study, the rat model of transient middle cerebral artery occlusion was used to explore the neuroprotective effect and underlying mechanisms of direct primary somatosensory (S1) cortex ES with an electric current of 20 Hz, 2 ms biphasic pulse, 100 μA for 30 min, starting at 30 min after reperfusion.Results: These results showed that S1 cortical ES after reperfusion decreased infarction volume and improved functional outcome. The number of activated microglia, astrocytes, and cleaved caspase-3 positive neurons after ischemia/reperfusion injury were reduced, demonstrating that S1 cortical ES alleviates inflammation and apoptosis. Brain-derived neurotrophic factor (BDNF) and phosphoinositide 3-kinase (PI3K)/Akt/mammalian target of rapamycin (mTOR) signaling pathway were upregulated in the penumbra area, suggesting that BDNF/TrkB signals and their downstream PI3K/Akt signaling pathway play roles in ES-related neuroprotection.Conclusion: This study demonstrates that somatosensory cortical ES soon after reperfusion can attenuate ischemia/reperfusion injury and is a promising adjuvant therapy for thrombolytic treatment after acute ischemic stroke. Advanced techniques and devices for high-definition transcranial direct current stimulation still deserve further development in this regard.

scholarly journals Blocking Free Radical Production via Adenoviral Gene Transfer Decreases Cardiac Ischemia–Reperfusion Injury

2000 ◽  
Vol 2 (5) ◽  
pp. 470-475 ◽  
Author(s):  
Henry L. Zhu ◽  
Allan S. Stewart ◽  
Matthew D. Taylor ◽  
C. Vijayasarathy ◽  
Timothy J. Gardner ◽  
...  
Keyword(s):  
Free Radical ◽  
Gene Transfer ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Ischemia ◽  
Free Radical Production ◽  
Adenoviral Gene Transfer ◽  
Radical Production

Effect of diazepam on the contents of amino acids and free radical during ischemia /reperfusion injury

2001 ◽  
Vol 21 (2) ◽  
pp. 102-104
Author(s):  
Hu Bo ◽  
Mei Yuanwu ◽  
Wei Guirong ◽  
Qiu Xiaoying ◽  
Sun Shenggang ◽  
...  
Keyword(s):  
Amino Acids ◽  
Free Radical ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion

scholarly journals Catestatin (Cst) protects the brain against ischemia/reperfusion injury through suppressing ER-stress and mitochondrial dysfunction

2020 ◽  
Author(s):  
Pei Bing ◽  
Chunjie Song ◽  
Zhengjiang Zhang ◽  
Shen Xin ◽  
Cui Qian
Keyword(s):  
Ischemic Stroke ◽  
Er Stress ◽  
Mitochondrial Dysfunction ◽  
Reperfusion Injury ◽  
Molecular Mechanisms ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Protective Function ◽  
The Brain

Abstract BackgroundCerebral stroke, known as a cerebral vascular accident (CVA), is one of the leading causes of long-term disability and the second leading cause of death worldwide. Despite amounts of advances that have been achieved in terms of the treatment of ischemic stroke. But thus far, clinically effective neuroprotectants remain elusive, which may mainly due to the lack of a complete understanding of molecular mechanisms of the stroke. Previous studies have been revealed that catestatin (Cst) is closely related to cardiovascular ischemia/reperfusion injuries. However, little is known about whether Cst is involved in the regulation of neuronal death processes during ischemia. MethodsIn the present study, we revealed a protective function of Cst on Rat neuron cell death in the setting of ischemia/reperfusion injury. ResultsWe found that Cst treatment significantly attenuated the deficits of hippocampal related behaviors. On mechanism, our data revealed that Cst administration remarkably reduced ER-stress and mitochondrial dysfunction caused by I/R injury, and subsequently protected brain cells from apoptosis. ConclusionIn sum, our results demonstrate that Cst ameliorates I/R injury-induced hippocampal-related behaviors deficits by protecting the neurons from I/R injury-induced ER-stress and mitochondrial dysfunction and apoptosis. Our findings may provide a promising novel neuroprotectant for ischemic stroke therapy.

scholarly journals Pien-Tze-Huang attenuates neuroinflammation in cerebral ischemia-reperfusion injury in rats partially through the TLR4/NF-κB/MAPK pathway

2021 ◽  
Author(s):  
Xiao-qin Zhang ◽  
Qing Zhang ◽  
Li-li Huang ◽  
Ming-zhen Liu ◽  
Zai-xing Cheng ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Protein Expressions ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Pien Tze Huang ◽  
Anti Inflammatory

Abstract Background Pien-Tze-Huang (PTH), one of the most famous traditional Chinese medicines in China, is traditionally applied to treat various inflammation-related diseases including stroke. However, literature regarding the anti-inflammatory effects and possible mechanisms of PTH in ischemic stroke is unavailable. This study intended to investigate the anti-inflammatory effects of PTH against cerebral ischemia-reperfusion injury and clarify its potential molecular mechanisms. Methods Cerebral ischemia-reperfusion injury was induced through transient left transient middle cerebral artery occlusion (MCAO) in male rats receiving oral pretreatment with PTH (180 mg/kg) for 4 days. TLR4 antagonist TAK-242 (3 mg/kg) was injected intraperitoneally at 1.5 h after MCAO. Magnetic resonance imaging, hematoxylin–eosin staining, RT-PCR, western blot, and immunofluorescence methods were used to studied the effect and mechanism of PTH against ischemic stroke. Results PTH treatment reduced cerebral infarct volume, improved neurological function, and ameliorated brain histopathological damage in MCAO rats. In addition, it markedly suppressed a variety of inflammatory responses as evidenced by the reduced mRNA levels of IL-1β, IL-6, TNF-α and MCP-1; the inhibition of microglia and astrocyte activations; and the decreased protein expressions of iNOS and COX-2 in injured brains. Moreover, PTH down-regulated the protein expressions of TLR4, MyD88, and TRAF6; reduced the expression and NF-κB; and lowered the protein expressions of p-ERK1/2, p-JNK, and p-p38. Similar effects were observed in the TAK-242 treated group. However, TAK-242 did not significantly reinforce the anti-inflammatory effects of PTH. Conclusion PTH could attenuate neuroinflammation, improve neurological function, and alleviate brain injury in MCAO rats, and its potential mechanisms are partly connected to inhibition of neuroinflammation involving the TLR4/NF-κB/MAPK signaling pathway.

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