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

Abstract

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.

• Authors: Zheng Liu, Wenwei Gao, Yuanqin Xu
• Journal: Bioengineered (Bioengineered) Vol. 13 Issue 5 Pg. 11718-11731 (05 2022) ISSN: 2165-5987 [Electronic] United States
• PMID: 35502892 (Publication Type: Journal Article)

Chemical References

• Glucosides
• Lignans
• eleutheroside E

Topics

• Animals
• Glucosides (pharmacology, therapeutic use)
• Lignans
• Rats
• Rats, Sprague-Dawley
• Reperfusion Injury (drug therapy, metabolism)