scholarly journals Effect of Exercise Preconditioning on Protein Expression of VEGF and NeuN in Rats with Cerebral Ischemia-reperfusion

2021 ◽  
Vol 31 (1) ◽  
pp. 37-43
Author(s):  
飞 裴 ◽  
雪冬 王 ◽  
宝龙 李 ◽  
强 唐 ◽  
路文 朱
Keyword(s):  
Cerebral Ischemia ◽  
Protein Expression ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Exercise Preconditioning

Methylphenidate exerts neuroprotective effects through the AMPK signaling pathway

2021 ◽  
pp. 096032712199602
Author(s):  
P Li ◽  
Y Huang ◽  
Y Yang ◽  
X Huang
Keyword(s):  
Cerebral Ischemia ◽  
Protein Expression ◽  
Cell Viability ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury ◽  
Brain Tissues

Purpose: Cerebral ischemia is the main cause of permanent adult disabilities worldwide. This study investigated the reparative effects and potential mechanisms of methylphenidate (MPH), a medication for the treatment of attention-deficit/hyperactivity disorder. Methods: In vitro oxygen-glucose deprivation/reperfusion (OGD/R) and in vivo cerebral ischemia-reperfusion models were established. Sprague-Dawley (SD) rats were randomly divided into four groups ( n = 20): Sham, Model, and MPH (0.5 and 1 mg/kg). Rats in MPH groups were treated with 0.5 or 1 mg/kg MPH via intraperitoneal injection for 7 days. Rats in the Sham and Model groups were treated with PBS during the same period. Cell viability was measured using MTT assay. Apoptosis was detected by Annexin V/PI staining. Protein expression was detected by Western blot. The volume of cerebral infarction was detected by triphenyltetrazolium chloride (TTC) staining. The DNA damage in ischemic brain tissues was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Results: MPH treatment significantly reduced OGD/R-induced cell damage, shown by the increased cell viability and decreased apoptotic rate. p-AMPK and p-ACC protein expression increased in the OGD/R model after MPH treatment. The addition of AMPK inhibitor largely abolished the neuroprotective effects of MPH, evidenced by the reduced cell viability, increased apoptotic rate, and decreased protein expression of p-AMPK as well as p-ACC. Moreover, MPH treatment significantly alleviated the cerebral ischemia-reperfusion injury and decreased apoptosis in brain tissues, which may be associated with the AMPK/ACC pathway. Conclusions: MPH exerted protective activities against oxidative stress in the OGD/R model and ameliorated brain damage of rats in the middle cerebral artery occlusion model, at least in part, through activating the AMPK pathway. These data demonstrated neuroprotective properties of MPH and highlighted it as a potential therapeutic agent against cerebral ischemia-reperfusion injury.

(Z)-7,4′-Dimethoxy-6-hydroxy-aurone- 4-O-β-glucopyranoside alleviates cerebral ischemia-reperfusion injury in rats associating with the regulation of JAK1/STAT1 signaling pathway

2020 ◽  
Vol 39 (11) ◽  
pp. 1507-1517
Author(s):  
R Du ◽  
X Zhou ◽  
D Yang ◽  
H Zhou ◽  
F Lin ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Protein Expression ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion ◽  
Janus Kinase ◽  
Terminal Deoxynucleotidyl Transferase ◽  
Enzyme Linked Immunosorbent Assay ◽  
Cerebral Ischemia Reperfusion ◽  
Brain Tissues

Inflammatory responses have been demonstrated to contribute to the neuronal death following cerebral ischemia. This study was to investigate the repairing effects and potential mechanisms of (Z)-7,4′-dimethoxy-6-hydroxy-aurone-4-O-β-glucopyranoside (DHAG), a compound with neuroprotective effects, on cerebral ischemia-reperfusion (I/R) injury in rats. Cerebral I/R model was established with middle cerebral artery occlusion method in Sprague Dawley rats and then rats were treated with DHAG (1 and 2 mg/kg) for 7 days. The volume of cerebral infarction was detected by triphenyltetrazolium chloride staining. The apoptosis in ischemic brain tissues was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling assay. Oxidative stress markers and inflammatory factors were detected by enzyme-linked immunosorbent assay. Protein expression was detected by Western blot. DHAG treatment significantly alleviated the cerebral I/R injury and decreased apoptosis in brain tissues. Moreover, DHAG treatment significantly inhibited oxidative stress and reduced inflammatory responses, associating with decreasing the protein expression of phosphorylated Janus kinase 1/phosphorylated signal transducer and transcriptional activator 1. These results demonstrated neuroprotective properties of DHAG and highlighted it as a potential therapeutic agent against injury of cerebral IR.

scholarly journals Tolerance-Inducing Dose of 3-Nitropropionic Acid Modulates bcl-2 and bax Balance in the Rat Brain: A Potential Mechanism of Chemical Preconditioning

2000 ◽  
Vol 20 (10) ◽  
pp. 1425-1436 ◽  
Author(s):  
Ansgar M. Brambrink ◽  
Armin Schneider ◽  
Holger Noga ◽  
Andreas Astheimer ◽  
Bernhard Götz ◽  
...  
Keyword(s):  
Single Dose ◽  
Cerebral Ischemia ◽  
Protein Expression ◽  
Ischemia Reperfusion ◽  
Global Cerebral Ischemia ◽  
Mrna Levels ◽  
Nitropropionic Acid ◽  
Bax Protein ◽  
Cerebral Ischemia Reperfusion ◽  
3 Nitropropionic Acid

Many studies have reported ischemia protection using various preconditioning techniques, including single dose 3-nitropropionic acid (3-NPA), a mitochondrial toxin. However, the cellular signal transduction cascades resulting in ischemic tolerance and the mechanisms involved in neuronal survival in the tolerant state still remain unclear. The current study investigated the mRNA and protein expression of the antiapoptotic bcl-2 and the proapoptotic bax, two antagonistic members of the bcl-2 gene family, in response to a single dose of 3-NPA, to global cerebral ischemia–reperfusion, and to the combination of both 3-NPA-pretreatment and subsequent global cerebral ischemia–reperfusion. Brain homogenates of adult Wistar rats (n = 25) were analyzed for bcl-2 and bax mRNA expression using a new highly sensitive and quantitative polymerase chain reaction (PCR) technique that allows real-time fluorescence measurements of the PCR product (LightCycler; Roche Diagnostics, Mannheim, Germany). Animals for mRNA analysis received 3-NPA (20 mg/kg, intraperitoneal; “chemical preconditioning”) or vehicle (normal saline), and were either observed for 24 plus 3 hours or were subjected to 15 minutes of global cerebral ischemia 24 hours after the pretreatment and observed for 3 hours of reperfusion. Immunohistochemistry was applied to serial brain sections of additional rats (n = 68) to determine amount and localization of the respective Bcl-2 and Bax protein expression in various brain areas. One set of animals was injected with 3-NPA and observed for 3, 12, 24, and 96 hours; a second set was exposed to 15 minutes global cerebral ischemia, 3, 12, and 24 hours reperfusion; and a third set was pretreated with 3-NPA or saline 24 hours before the ischemic brain insult and observed for 96 hours of reperfusion. The authors found single dose 3-NPA treatment to be associated with an elevated bcl-2:bax ratio (increased bcl-2 expression, decreased bax expression), both on the transcriptional (mRNA) and the translational (protein) level. The differential influence of 3-NPA was maintained during early recovery from global cerebral ischemia (3 hours), when 3-NPA pretreated animals showed higher bcl-2 and lower bax mRNA levels compared with rats with saline treatment. Respective changes in protein expression were localized predominately in neurons vulnerable to ischemic damage. Compared with baseline, Bcl-2 protein was significantly higher in surviving neurons at 96 hours after the insult, whereas Bax protein remained unchanged. However, at this late time of postischemic recovery (96 hours), the protein expression pattern of surviving neurons was not different between animals with and without 3-NPA pretreatment. To the authors' knowledge, the current study is the first report on the differential expression of pro-and antiapoptotic genes after a single, nonlethal dose of 3-NPA. The current results suggest alterations in the balance between pro-and antiapoptotic proteins as a potential explanation for the reported protection provided by chemical preconditioning using 3-NPA in rats.

Ephedrine attenuates cerebral ischemia/reperfusion injury in rats through NF-κB signaling pathway

2020 ◽  
pp. 096032712097545
Author(s):  
Chanhong Shi ◽  
Jianhong Li ◽  
Jianwei Li
Keyword(s):  
Cerebral Ischemia ◽  
Protein Expression ◽  
Reperfusion Injury ◽  
Rat Model ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Infarct Volume ◽  
Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

The inflammation and immune responses are critical in ischemic stroke and contribute to aggravated brain damage. Ephedrine was reported to play an important role in the control of inflammatory responses. This study was to investigate the repairing effects and potential mechanisms of ephedrine on cerebral ischemic injury in a rat model of focal cerebral ischemia. The rat model of cerebral ischemia/reperfusion injury was established using the middle cerebral artery occlusion (MCAO) method and then rats were treated with ephedrine (5 and 10 mg/kg) for 7 days. The neurobehavioral progression was assessed using the neurological scoring method. The pathology of brain tissue was evaluated by hematoxylin and eosin (H&E) staining. The infarct volume was examined by triphenyltetrazolium chloride (TTC) staining. The apoptosis in ischemic brain tissues was detected by terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL) assay. Inflammatory factors were detected by enzyme-linked immunosorbent assay (ELISA). Gene quantification and protein expression were detected by real-time PCR and western blot, respectively. Ephedrine treatment significantly alleviated the cerebral ischemia/reperfusion injury, evidenced by decreased neurological deficit score, infarct volume and water content. Ephedrine also decreased autophagy and apoptosis in brain tissues. Moreover, ephedrine treatment significantly reduced inflammatory responses, associating with decreasing the protein expression of p-NF-κB. These results demonstrated neuroprotective properties of ephedrine and highlighted it as a new potential anti-inflammatory agent against injury of cerebral ischemia/reperfusion.

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.

scholarly journals Selective brain hypothermia ameliorates focal cerebral ischemia-reperfusion injury via inhibiting Fis1 in rats

2019 ◽  
Author(s):  
Yanan Tang ◽  
Huailong Chen ◽  
Xiaopeng Sun ◽  
Weiwei Qin ◽  
Fei Shi ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Protein Expression ◽  
Mrna Expression ◽  
Normal Saline ◽  
Neuronal Apoptosis ◽  
Focal Cerebral Ischemia ◽  
Ischemia Reperfusion ◽  
Mitochondrial Fission ◽  
C Protein ◽  
Cerebral Ischemia Reperfusion

AbstractMitochondrial immoderate fission induces neuronal apoptosis following focal cerebral ischemia-reperfusion (I/R) injury. With fewer complications, selective brain hypothermia (SBH) is considered an effective treatment against neuronal injury after stroke. However, the specific mechanism by which SBH influences mitochondrial fission remains unknown. Mitochondrial fission 1 protein (Fis1), a key factor of the mitochondrial fission system, regulates mitochondrial dynamics. This study aimed to investigate whether SBH regulates Fis1 expression in focal cerebral I/R injury. In this study, rat middle cerebral artery occlusion (MCAO) models were established. After 2 h of occlusion, cold saline or normal saline was pumped into rats in different groups through the carotid artery, followed by restoration of blood perfusion. Cortical and rectal temperatures showed that the cold saline treatment achieved SBH. Cerebral I/R injury increased neurological deficit scores (NDS); neuronal apoptosis; Fis1 protein and mRNA expression; cytosolic cytochrome c (cyto-Cyto c) protein expression at 6, 24 and 48 h postreperfusion; and cerebral infarct volumes at 24 h postreperfusion. Interestingly, SBH inhibited Fis1 protein and mRNA expression, blocked cyto-Cyto c protein expression, preserved neuronal cell integrity, and reduced neuronal apoptosis. However, normal saline treatment rarely resulted in positive outcomes. Based on these results, SBH inhibited Fis1 expression, thus ameliorating focal cerebral I/R injury in rats.

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