Eleutheroside E alleviates cerebral ischemia-reperfusion injury in a 5-hydroxytryptamine receptor 2C (Htr2c)-dependent manner in rats

Stroke is the central disorder underlined by ischemia-reperfusion (I/R) injury. Eleutheroside E (EE) is administered as the shield in some ischemia tissues with anti-inflammatory action. However, whether EE defends I/R-induced damage in the brain remains unknown. Here, we demonstrated that EE signif...

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Bibliographic Details
Published in:Bioengineered 2022-05, Vol.13 (5), p.11718-11731
Main Authors: Liu, Zheng, Gao, Wenwei, Xu, Yuanqin
Format: Article
Language:English
Subjects:
Animals
apoptosis
eleutheroside E
Glucosides - pharmacology
Glucosides - therapeutic use
htr2c
Ischemia-reperfusion
Lignans
rat hippocampal neuron
Rats
Rats, Sprague-Dawley
Reperfusion Injury - drug therapy
Reperfusion Injury - metabolism
Research Paper
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Summary:Stroke is the central disorder underlined by ischemia-reperfusion (I/R) injury. Eleutheroside E (EE) is administered as the shield in some ischemia tissues with anti-inflammatory action. However, whether EE defends I/R-induced damage in the brain remains unknown. Here, we demonstrated that EE significantly alleviated the cerebral I/R injury and reduced the apoptosis of hippocampal neuron cells in rats. During the anti-apoptosis process, EE significantly upregulated the expression of 5-hydroxytryptamine receptor 2C (Htr2c) gene. Silencing Htr2c expression dramatically weakened the protective effect of EE on I/R-induced apoptosis of rat hippocampal neuron. EE-regulated Htr2c also remarkably inhibited the expression of caspase-3, −6 and −7, thereby suggesting a plausible anti-apoptosis mechanism associated with Htr2c/caspase axis. These findings elicit the potentially clinical strategy that targets Htr2c to improve outcome of ischemia brain.
ISSN:2165-5979
2165-5987
DOI:10.1080/21655979.2022.2071009