scholarly journals Epigallocatechin-3-Gallate Reduces Neuronal Apoptosis in Rats after Middle Cerebral Artery Occlusion Injury via PI3K/AKT/eNOS Signaling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-9 ◽  
Author(s):  
Wang Nan ◽  
Xu Zhonghang ◽  
Chen Keyan ◽  
Liu Tongtong ◽  
Guo Wanshu ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Brain Injury ◽  
Protective Effect ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Signaling Pathway ◽  
Neuronal Apoptosis ◽  
Artery Occlusion ◽  
Rat Models ◽  
Cerebral Artery Occlusion

Background/Aims. Epigallocatechin-3-gallate (EGCG) has neuroprotective effects and the ability to resist amyloidosis. This study observed the protective effect of EGCG against neuronal injury in rat models of middle cerebral artery occlusion (MCAO) and investigated the mechanism of action of PI3K/AKT/eNOS signaling pathway. Methods. Rat models of permanent MCAO were established using the suture method. Rat behavior was measured using neurological deficit score. Pathology and apoptosis were measured using HE staining and TUNEL. Oxidative stress and brain injury markers were examined using ELISA. Apoptosis-related proteins and PI3K/AKT/eNOS signaling pathway were determined using western blot assay and immunohistochemistry. Results. EGCG decreased neurological function score, protected nerve cells, inhibited neuronal apoptosis, and inhibited oxidative stress injury and brain injury markers level after MCAO. EGCG reduced the apoptotic rate of neurons, increased the expression of Bcl-2, and decreased the expression of Caspase-3 and Bax. After LY294002 suppressed the PI3K pathway, the protective effect of EGCG decreased after administration of PI3K inhibitors. Conclusion. EGCG has a protective effect on rat brain injury induced by MCAO, possibly by modulating the PI3K/AKT/eNOS signaling pathway.

scholarly journals Apocynin promotes neural function recovery and suppresses neuronal apoptosis by inhibiting Tlr4/NF-κB signaling pathway in a rat model of cerebral infarction

2018 ◽  
Vol 32 ◽  
pp. 205873841881770
Author(s):  
Lemen Pan ◽  
Shuxia Qian
Keyword(s):  
Oxidative Stress ◽  
Inflammatory Response ◽  
Cerebral Infarction ◽  
Middle Cerebral Artery ◽  
Middle Cerebral Artery Occlusion ◽  
Cerebral Artery ◽  
Neuronal Apoptosis ◽  
Artery Occlusion ◽  
Cerebral Artery Occlusion ◽  
And Oxidative Stress

Occlusion of arteries in the brain is a common cause of cerebral infarction which induces inflammatory response and oxidative stress resulting in neuronal apoptosis and disruption of neurological function. The present study investigated the protective roles of an nicotinamide adenine dinucleotide phosphate oxidase inhibitor, apocynin, against cerebral infarction. Rat went through a surgery of middle cerebral artery occlusion and a subset of rats was treated with apocynin by intraperitoneal injection. The volume of cerebral infarction and water content were measured. Neuronal apoptosis, inflammatory response, and oxidative stress were assessed following middle cerebral artery occlusion and apocynin treatment. We found that apocynin significantly improved neurological function, increased forelimb placement test scores, and suppressed balance beam walk latency in rats with cerebral infarction. Histological and biochemistry analysis revealed that apocynin lead to a significant reduction in the volume of cerebral infarction as well as cerebral water content, suppressed neuronal apoptosis, oxidative stress, and inflammatory response induced by middle cerebral artery occlusion. Finally, we found that apocynin suppressed Tlr4/nuclear factor-k-gene binding signaling pathway that was upregulated in rats with cerebral infarction. Our results indicate that apocynin may represent a potent therapeutic strategy in alleviating neurological dysfunctions in patients with cerebral infarction.

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