Do RAS Inhibitors Protect the Brain from Cerebral Ischemic Injury?

2013 ◽  
Vol 9 (2) ◽  
pp. 86-92 ◽  
Author(s):  
Naohisa Hosomi ◽  
Akira Nishiyama ◽  
Masayasu Matsumoto
Keyword(s):  
Ischemic Injury ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic ◽  
The Brain ◽  
Ras Inhibitors

scholarly journals Resveratrol Protects against Cerebral Ischemic Injury via Restraining Lipid Peroxidation, Transition Elements, and Toxic Metal Levels, but Enhancing Anti-Oxidant Activity

Antioxidants ◽  
2021 ◽  
Vol 10 (10) ◽  
pp. 1515
Author(s):  
Ming-Cheng Lin ◽  
Chien-Chi Liu ◽  
Yu-Chen Lin ◽  
Chin-Sheng Liao
Keyword(s):  
Lipid Peroxidation ◽  
Cerebral Ischemia ◽  
Toxic Metals ◽  
Ischemic Injury ◽  
Transition Elements ◽  
Anti Oxidant ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic ◽  
The Right ◽  
The Brain

Cerebral ischemia is related to increased oxidative stress. Resveratrol displays anti-oxidant and anti-inflammatory properties. The transition elements iron (Fe) and copper (Cu) are indispensable for the brain but overload is deleterious to brain function. Aluminum (Al) and arsenic (As) are toxic metals that seriously threaten brain health. This study was conducted to elucidate the correlation of the neuroprotective mechanism of resveratrol to protect cerebral ischemic damage with modulation of the levels of lipid peroxidation, anti-oxidants, transition elements, and toxic metals. Experimentally, 20 mg/kg of resveratrol was given once daily for 10 days. The cerebral ischemic operation was performed via occlusion of the right common carotid artery together with the right middle cerebral artery for 60 min followed by homogenization of the brain cortex and collection of supernatants for biochemical analysis. In the ligation group, levels of malondialdehyde, Fe, Cu, Al, and As increased but those of the anti-oxidants superoxide dismutase and catalase decreased. Pretreating rats with resveratrol before ischemia significantly reversed these effects. Our findings highlight the association of overload of Fe, Cu, As, and Al with the pathophysiology of cerebral ischemia. In conclusion, resveratrol protects against cerebral ischemic injury via restraining lipid peroxidation, transition elements, and toxic metals, but increasing anti-oxidant activity.

scholarly journals The Association of Suppressed Hypoxia-Inducible Factor-1 Transactivation of Angiogenesis With Defective Recovery From Cerebral Ischemic Injury in Aged Rats

2021 ◽  
Vol 13 ◽  
Author(s):  
Yingjia Guo ◽  
Junpeng Zhou ◽  
Xianglong Li ◽  
Ying Xiao ◽  
Jingyao Zhang ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Hypoxia Inducible Factor ◽  
Young Patients ◽  
Ischemic Injury ◽  
Aged Rats ◽  
Transcription Activity ◽  
Hypoxia Inducible Factor 1 ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic ◽  
The Brain

Elderly patients suffer more brain damage in comparison with young patients from the same ischemic stroke. The present study was undertaken to test the hypothesis that suppressed hypoxia-inducible factor-1 (HIF-1) transcription activity is responsible for defective recovery after ischemic stroke in the elders. Aged and young rats underwent 1-h transient middle cerebral artery occlusion (MCAO) to produce cerebral ischemic injury. The initial cerebral infarct volume in the young gradually declined as time elapsed, but in the aged rats remained the same. The defective recovery in the aged was associated with depressed angiogenesis and retarded neurorestoration. There was no difference in HIF-1α accumulation in the brain between the two age groups, but the expression of HIF-1 regulated genes involved in cerebral recovery was suppressed in the aged. In confirmation, inhibition of HIF-1 transactivation of gene expression in the young suppressed cerebral recovery from MCAO as the same as that observed in the aged rats. Furthermore, a copper metabolism MURR domain 1 (COMMD1) was significantly elevated after MCAO only in the brain of aged rats, and suppression of COMMD1 by siRNA targeting COMMD1 restored HIF-1 transactivation and improved recovery from MCAO-induced damage in the aged brain. These results demonstrate that impaired HIF-1 transcription activity, due at least partially to overexpression of COMMD1, is associated with the defective cerebral recovery from ischemic stroke in the aged rats.

scholarly journals Study on the Mechanism of mTOR-Mediated Autophagy during Electroacupuncture Pretreatment against Cerebral Ischemic Injury

2016 ◽  
Vol 2016 ◽  
pp. 1-8 ◽  
Author(s):  
Zhou-Quan Wu ◽  
Su-yang Cui ◽  
Liang Zhu ◽  
Zhi-qing Zou
Keyword(s):  
Pearson Correlation ◽  
Specific Inhibitor ◽  
Ischemic Injury ◽  
Artery Occlusion ◽  
Protective Effects ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic ◽  
Cerebral Artery Occlusion ◽  
The Impact ◽  
The Brain

This study is aimed at investigating the association between the electroacupuncture (EA) pretreatment-induced protective effect against early cerebral ischemic injury and autophagy. EA pretreatment can protect cerebral ischemic and reperfusion injuries, but whether the attenuation of early cerebral ischemic injury by EA pretreatment was associated with autophagy is not yet clear. This study used the middle cerebral artery occlusion model to monitor the process of ischemic injury. For rats in the EA pretreatment group, EA pretreatment was conducted at Baihui acupoint before ischemia for 30 min for 5 consecutive days. The results suggested that EA pretreatment significantly increased the expression of autophagy in the cerebral cortical area on the ischemic side of rats. But the EA pretreatment-induced protective effects on the brain could be reversed by the specific inhibitor 3-methyladenine of autophagy. Additionally, the Pearson correlation analysis indicated that the impact of EA pretreatment on p-mTOR (2481) was negatively correlated with its impact on autophagy. In conclusion, the mechanism of EA pretreatment at Baihui acupoint against cerebral ischemic injury is mainly associated with the upregulation of autophagy expression, and its regulation of autophagy may depend on mTOR-mediated signaling pathways.

scholarly journals Intradialytic Cerebral Hypoperfusion as Mechanism for Cognitive Impairment in Patients on Hemodialysis

2019 ◽  
Vol 30 (11) ◽  
pp. 2052-2058 ◽  
Author(s):  
Dawn F. Wolfgram
Keyword(s):  
Cognitive Impairment ◽  
Cerebral Perfusion ◽  
Ischemic Injury ◽  
Hemodialysis Patients ◽  
Cognitive Outcomes ◽  
Cerebral Injury ◽  
Cerebral Hypoperfusion ◽  
Increased Risk ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

The high frequency of cognitive impairment in individuals on hemodialysis is well characterized. In-center hemodialysis patients are disproportionately affected by cognitive impairment compared with other dialysis populations, identifying hemodialysis itself as a possible factor. The pathophysiology of cognitive impairment has multiple components, but vascular-mediated cerebral injury appears to contribute based on studies demonstrating increased cerebral ischemic lesions and atrophy in brain imaging of patients on hemodialysis. Patients on hemodialysis may be at increased risk for cerebral ischemic injury disease due to vasculopathy associated with ESKD and from their comorbid diseases, such as hypertension and diabetes. This review focuses on the intradialytic cerebral hypoperfusion that can occur during routine hemodialysis due to the circulatory stress of hemodialysis. This includes a review of current methods used to monitor intradialytic cerebral perfusion and the structural and functional cognitive outcomes that have been associated with changes in intradialytic cerebral perfusion. Monitoring of intradialytic cerebral perfusion may become clinically relevant as nephrologists try to avoid the cognitive complications seen with hemodialysis. Identifying the appropriate methods to assess risk for cerebral ischemic injury and the relationship of intradialytic cerebral hypoperfusion to cognitive outcomes will help inform the decision to use intradialytic cerebral perfusion monitoring in the clinical setting as part of a strategy to prevent cognitive decline.

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