scholarly journals Restoration of L-OPA1 alleviates acute ischemic stroke injury in rats via inhibiting neuronal apoptosis and preserving mitochondrial function

Redox Biology ◽  
2020 ◽  
Vol 34 ◽  
pp. 101503 ◽  
Author(s):  
Yongxing Lai ◽  
Peiqiang Lin ◽  
Manli Chen ◽  
Yixian Zhang ◽  
Jianhao Chen ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Mitochondrial Function ◽  
Neuronal Apoptosis

The role of elevated levels of microRNA-155-5p and microRNA-124-5p in hyperuricemia and acute ischemic stroke

2021 ◽  
Vol 11 (10) ◽  
pp. 1674-1680
Author(s):  
Yuan Yao ◽  
Jun Yuan ◽  
Yanju Ma ◽  
Runxiu Zhu ◽  
Yong Ma
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Clinical Application ◽  
Cerebral Vasospasm ◽  
Rat Model ◽  
Inner Mongolia ◽  
Neuronal Apoptosis ◽  
Projection Neuron ◽  
Neuron Differentiation

Hyperuricemia is closely related to acute ischemic stroke (AIS). In our study, we investigated the pattern of miRNA-155-5p and miRNA-124-5p expressions along with its clinical application in AIS and hyperuricemia patients and in a hyperuricemia rat model by RT-qPCR. The hyperuricemia rat model was established, and we found that the levels of miRNA-155-5p and miRNA-124-5p were increased in the serum, brain and kidney tissues compared with those in the normal rats. We proved that the levels of miRNA-155-5p and miRNA-124-5p were also elevated in AIS, hyperuricemia and AIS accompanied with hyperuricemia patients enrolled from the department of neurology in Inner Mongolia People’s Hospital (IMPH). The miRNA-155-5p and miRNA-124-5p were mainly associated with neuronal apoptosis, cerebral vasospasm, neuron projection, neuron projection morphogenesis, neuron differentiation and exocytosis. The above results might provide clues for the study the pathogenesis of AIS and hyperuricemia.

scholarly journals YiQiFuMai Powder Injection Protects against Ischemic Stroke via Inhibiting Neuronal Apoptosis and PKCδ/Drp1-Mediated Excessive Mitochondrial Fission

2017 ◽  
Vol 2017 ◽  
pp. 1-17 ◽  
Author(s):  
Yingqiong Xu ◽  
Yan Wang ◽  
Guangyun Wang ◽  
Xinyi Ye ◽  
Jiangwei Zhang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Ischemic Stroke ◽  
Mitochondrial Dysfunction ◽  
Mitochondrial Function ◽  
Neuronal Apoptosis ◽  
Mitochondrial Fission ◽  
Powder Injection ◽  
Mitochondria Membrane Potential ◽  
Protein Levels ◽  
Underlying Mechanisms

YiQiFuMai (YQFM) powder injection has been reported to be used in cardiovascular and nervous system diseases with marked efficacy. However, as a treatment against diseases characterized by hypoxia, lassitude, and asthenia, the effects and underlying mechanisms of YQFM in neuronal mitochondrial function and dynamics have not been fully elucidated. Here, we demonstrated that YQFM inhibited mitochondrial apoptosis and activation of dynamin-related protein 1 (Drp1) in cerebral ischemia-injured rats, producing a significant improvement in cerebral infarction and neurological score. YQFM also attenuated oxidative stress-induced mitochondrial dysfunction and apoptosis through increasing ATP level and mitochondria membrane potential (Δψm), inhibiting ROS production, and regulating Bcl-2 family protein levels in primary cultured neurons. Moreover, YQFM inhibited excessive mitochondrial fission, Drp1 phosphorylation, and translocation from cytoplasm to mitochondria induced by oxidative stress. We provided the first evidence that YQFM inhibited the activation, association, and translocation of PKCδ and Drp1 upon oxidative stress. Taken together, we demonstrate that YQFM ameliorates ischemic stroke-induced neuronal apoptosis through inhibiting mitochondrial dysfunction and PKCδ/Drp1-mediated excessive mitochondrial fission. These findings not only put new insights into the unique neuroprotective properties of YQFM associated with the regulation of mitochondrial function but also expand our understanding of the underlying mechanisms of ischemic stroke.

Pien-Tze-Huang protects cerebral ischemic injury by inhibiting neuronal apoptosis in acute ischemic stroke rats

2018 ◽  
Vol 219 ◽  
pp. 117-125 ◽  
Author(s):  
Xiaoqin Zhang ◽  
Yiping Zhang ◽  
Songqi Tang ◽  
Lishuang Yu ◽  
Youqin Zhao ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Neuronal Apoptosis ◽  
Ischemic Injury ◽  
Pien Tze Huang ◽  
Cerebral Ischemic Injury ◽  
Cerebral Ischemic

scholarly journals Intracarotid Transplantation of Skin-Derived Precursor Schwann Cells Promotes Functional Recovery After Acute Ischemic Stroke in Rats

2021 ◽  
Vol 12 ◽  
Author(s):  
Jingjing Liang ◽  
Ronghui Cui ◽  
Jinglei Wang ◽  
Jiabing Shen ◽  
Ying Chen ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Acute Ischemic Stroke ◽  
Schwann Cells ◽  
Functional Recovery ◽  
Cortical Neurons ◽  
Neuronal Apoptosis ◽  
Infarct Volume ◽  
Tunel Staining ◽  
Primary Cortical Neurons

Purpose: Skin-derived Precursor Schwann cells (SKP-SCs) have been reported to provide neuroprotection for the injured and dysmyelinated nervous system. However, little is known about SKP-SCs on acute ischemic stroke (AIS). We aimed to explore the efficacy and the potential mechanism of action of SKP-SCs on AIS in a rat ischemic stroke model.Methods: Adult male Sprague–Dawley rats were subjected to a middle cerebral artery occlusion (MCAO) for 1.5 h on Day 0 and subsequently received an intracarotid injection of 2 × 106 green fluorescent protein (GFP) -labeled SKP-SCs or phosphate buffered saline (PBS) during reperfusion. Neurological function was assessed by behavioral tests on Days 1, 4, 7, 14, and 28. In a satellite cohort, rat brains were harvested and infarct volume was measured with 2,3,5-triphenyltetrazolium chloride (TTC) staining on Days 1 and 7, and migration and survival of SKP-SCs in the brain were traced by monitoring green fluorescence at 6 and12 h on Day 0, and on Days 1, 4, 7, 14, and 28. Histopathology and immunofluorescence staining were used to analyze the morphology, survival and apoptosis of neurons. Additionally, in an in vitro SKP-SC co-culture model using fetal rat primary cortical neurons underwent oxygen glucose deprivation/reoxygenation (OGD/R), Western blot was used to detect the expression of apoptosis indicators including activated caspase-3, Bax, and Bcl-2. TUNEL staining was used to count apoptotic cells.Results: Intracarotid transplantation of SKP-SCs effectively migrated to the periinfarct area and survived for at least 4 weeks. Transplanted SKP-SCs inhibited neuronal apoptosis, reduced infarct volume, and improved neurological recovery in the MCAO rats. Moreover, in vitro data showed that SKP-SCs treatment inhibited OGD/R-induced neuronal apoptosis and promoted survival of the cultured primary cortical neurons.Conclusions: Intracarotid transplantation of SKP-SCs promoted functional recovery in the rat AIS model and possesses the potential to be further developed as a novel therapy to treat ischemic stroke in humans.

Predictive value of the ankle brachial index in patients with acute ischemic stroke

VASA ◽  
2014 ◽  
Vol 43 (1) ◽  
pp. 55-61 ◽  
Author(s):  
Konstantinos Tziomalos ◽  
Vasilios Giampatzis ◽  
Stella Bouziana ◽  
Athinodoros Pavlidis ◽  
Marianna Spanou ◽  
...  
Keyword(s):  
Ischemic Stroke ◽  
Hospital Mortality ◽  
Acute Ischemic Stroke ◽  
Ankle Brachial Index ◽  
Arterial Disease ◽  
National Institutes Of Health ◽  
Limited Data ◽  
Severe Stroke ◽  
Hospital Outcome ◽  
Peripheral Arterial

Background: Peripheral arterial disease (PAD) is frequently present in patients with acute ischemic stroke. However, there are limited data regarding the association between ankle brachial index (ABI) ≤ 0.90 (which is diagnostic of PAD) or > 1.40 (suggesting calcified arteries) and the severity of stroke and in-hospital outcome in this population. We aimed to evaluate these associations in patients with acute ischemic stroke. Patients and methods: We prospectively studied 342 consecutive patients admitted for acute ischemic stroke (37.4 % males, mean age 78.8 ± 6.4 years). The severity of stroke was assessed with the National Institutes of Health Stroke Scale (NIHSS)and the modified Rankin scale (mRS) at admission. The outcome was assessed with the mRS and dependency (mRS 2 - 5) at discharge and in-hospital mortality. Results: An ABI ≤ 0.90 was present in 24.6 % of the patients whereas 68.1 % had ABI 0.91 - 1.40 and 7.3 % had ABI > 1.40. At admission, the NIHSS score did not differ between the 3 groups (10.4 ± 10.6, 8.3 ± 9.3 and 9.3 ± 9.4, respectively). The mRS score was also comparable in the 3 groups (3.6 ± 1.7, 3.1 ± 1.8 and 3.5 ± 2.3, respectively). At discharge, the mRS score did not differ between the 3 groups (2.9 ± 2.2, 2.3 ± 2.1 and 2.7 ± 2.5, respectively) and dependency rates were also comparable (59.5, 47.6 and 53.3 %, respectively). In-hospital mortality was almost two-times higher in patients with ABI ≤ 0.90 than in patients with ABI 0.91 - 1.40 or > 1.40 but this difference was not significant (10.9, 6.6 and 6.3 %, respectively). Conclusions: An ABI ≤ 0.90 or > 1.40 does not appear to be associated with more severe stroke or worse in-hospital outcome in patients with acute ischemic stroke.

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