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Salidroside Restores an Anti-inflammatory Endothelial Phenotype by Selectively Inhibiting Endothelial Complement
1Centre of Biomedical Research & Development, Fujian University of Traditional Chinese Medicine, No. 1 Huatou Road, Minhou Shangjie, Fuzhou, China.
Inflammation
|November 9, 2019
Summary
Salidroside from Rhodiola rosea protects brain cells by inhibiting complement activation in endothelial cells, reducing inflammation and neuronal damage after stroke. This study clarifies its mechanism in cerebral ischemia-reperfusion injury.
Area of Science:
- Neuroscience
- Immunology
- Pharmacology
Background:
- Salidroside, derived from Rhodiola rosea, shows promise in mitigating inflammation and neuronal damage following cerebral ischemia-reperfusion.
- Its precise mechanism, particularly regarding the inhibition of complement system activation, remains incompletely understood.
Purpose of the Study:
- To investigate the cellular targets and mechanisms by which salidroside inhibits complement activation in the brain.
- To elucidate the role of endothelial cells in salidroside's protective effects against oxidative stress.
Main Methods:
- Utilized oxygen-glucose deprivation/restoration (OGD/R) in human umbilical endothelial cells (HUVEC), astrocytes, and microglial BV2 cells.
- Assessed complement component C3 activation, inflammatory markers (VCAM-1, ICAM-1, P-selectin, E-selectin), complement regulatory proteins (CD46, CD59), and apoptosis markers (Bcl-2/Bax ratio).
- Evaluated salidroside's effects in a rat model of middle cerebral artery occlusion (MCAO) with reperfusion.
Main Results:
- Salidroside inhibited OGD/R-induced C3 activation and complement component increases specifically in HUVEC, not in astrocytes or microglia.
- It restored anti-inflammatory endothelial phenotypes by upregulating CD46/CD59 and downregulating adhesion molecules in HUVEC.
- Salidroside reduced endothelial activation, neutrophil adhesion, and brain inflammation in MCAO rats, mirroring effects of C3a receptor antagonists.
Conclusions:
- Endothelial cells are a key site for salidroside's complement inhibitory action during cerebral ischemia-reperfusion.
- Salidroside restores an anti-inflammatory and anti-apoptotic endothelial state, contributing to neuroprotection.
- These findings highlight salidroside as a potential therapeutic agent for ischemic stroke by targeting endothelial complement pathways.
