Neuroprotective effects of olprinone after cerebral ischemia/reperfusion injury in rats

2011 ◽  
Vol 503 (2) ◽  
pp. 93-99 ◽  
Author(s):  
Tiziana Genovese ◽  
Emanuela Mazzon ◽  
Irene Paterniti ◽  
Emanuela Esposito ◽  
Salvatore Cuzzocrea
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

The Mechanism of Gastrodin Participating in Improving the Cerebral Ischemia-Reperfusion Injury Through Notch 1 and NF-κB Signaling Pathways

2021 ◽  
Vol 11 (2) ◽  
pp. 271-275
Author(s):  
Qing Hong ◽  
Junqiang Ye ◽  
Xijia Wang ◽  
Chao Zhang
Keyword(s):  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Signaling Pathways ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Brain Area ◽  
Notch 1 ◽  
Neuroprotective Effects ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Background: The purpose of this study was to investigate whether Gastrodin can activate the Notch 1 signaling pathway in the ischemic brain area to produce neuroprotective effects against cerebral ischemia-reperfusion injury, and to elucidate the role of Notch 1 and NF-κB signaling pathways in the Gastrodin-induced cerebral ischemic tolerance. Material and methods: The focal cerebral ischemia reperfusion model of middle cerebral artery embolism was established. TTC staining was applied to detect cerebral infarction. Tunel/NeuN immunofluorescence double labeling was employed to detect apoptosis. WB was used to detect the expressions of proteins related to the Notch 1 and NF-κB pathways. Results: Gastrodin can reduce neuron apoptosis in hippocampus after MCAO/R injury. After DAPT blocked Notch 1 signaling, the neuroprotective effects of Gastrodin improving neural function score, reducing cerebral infarction volume, and inhibiting neuronal apoptosis, were all reversed. Compared with the MCAO/R group, DAPT blocking Notch 1 signaling can also improve the neurological score of rats after MCAO/R injury, reduce cerebral infarct volume, and reduce neuronal apoptosis. Gastrodin can activate Notch 1 and NF-κB signaling pathways in cerebral ischemic areas and increase the expression of related proteins. After DAPT inhibited the Notch 1 signaling in the ipsilateral brain region, the phosphorylation level was significantly decreased, indicating that the activity of the NF-κB pathway was regulated by the Notch 1 signaling. Conclusion: Gastrodin-mediated protection against cerebral ischemia-reperfusion injury is related to the activation of Notch 1 signaling and the up-regulation of NF-κB signaling pathway activity in neurons of ischemic brain area.

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.

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