scholarly journals Asiaticoside Alleviates Cerebral Ischemia-Reperfusion Injury via NOD2/Mitogen-Activated Protein Kinase (MAPK)/Nuclear Factor kappa B (NF-κB) Signaling Pathway

2020 ◽  
Vol 26 ◽  
Author(s):  
Chunhui Zhang ◽  
Suyan Chen ◽  
Zhenxiang Zhang ◽  
Hui Xu ◽  
Weihong Zhang ◽  
...  
Keyword(s):  
Cerebral Ischemia ◽  
Protein Kinase ◽  
Nuclear Factor Kappa B ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mitogen Activated Protein Kinase ◽  
Nuclear Factor ◽  
Cerebral Ischemia Reperfusion ◽  
Mitogen Activated Protein ◽  
Cerebral Ischemia Reperfusion Injury

Diosmetin Ameliorates Cerebral Ischemia/Reperfusion Injury in PC12 Cells Through Nuclear Factor-kB (NF-kB) and Nuclear Factor Erythroid 2-Related Factor/Heme Oxygenase-1 (Nrf 2/HO-1) Pathway

2019 ◽  
Vol 17 (3) ◽  
pp. 322-328
Author(s):  
Luan Lan ◽  
Cao Lanxiu ◽  
Zhu Lei ◽  
Sun Jianhua
Keyword(s):  
Oxidative Stress ◽  
Cerebral Ischemia ◽  
Reperfusion Injury ◽  
Pc12 Cells ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Nuclear Factor ◽  
Oxygen Species ◽  
Cerebral Ischemia Reperfusion ◽  
Cerebral Ischemia Reperfusion Injury

Diosmetin, a natural flavonoid, exhibits a variety of pharmacologic activities including inhibition of inflammation and oxidation. Therefore, its potential role in the management of cerebral ischemia/reperfusion (I/R) injury remains to be examined. In this study, we explored the underlying molecular mechanisms of diosmetin effects on cerebral ischemia/reperfusion injury in vitro. The results show that hypoxia/reoxygenation treatment of PC12 cells decreased cell viability and increased apoptosis, inflammation and oxidative stress. Diosmetin improved cellular viability, decreased lactate dehydrogenase release, and inhibited apoptosis in hypoxia-/reoxygenation-treated PC12 cells. Furthermore, diosmetin effectively inhibited the NF-kB signaling pathway to attenuate the inflammatory response. Also, diosmetin inhibited reactive oxygen species generation to attenuate I/R injury-induced oxidative stress in PC12 cells probably through the activation of Nrf 2/HO-1 pathway. Therefore, diosmetin effectively protected cells from I/R injury in nerve cells by scavenging reactive oxygen species by activating Nrf 2/HO-1 pathway and inhibiting inflammation by the suppression of NF-kB signaling pathway. Diosmetin can be regarded as a potential agent for cerebral ischemia/reperfusion injury treatment.

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