Salidroside Reduces Inflammation and Brain Injury After Permanent Middle Cerebral Artery Occlusion in Rats by
1Centre of Biomedical Research & Development, Fujian University of Traditional Chinese Medicine, No. 1 Huatou Road, Minhou Shangjie, Fuzhou, China.
Inflammation
|June 24, 2019
Summary
Salidroside effectively reduced brain damage and neurological deficits in a rat stroke model. This neuroprotection is linked to the PI3K/PKB/Nrf2/NFκB pathway, not complement C3.
Area of Science:
- Neuroscience
- Pharmacology
- Biochemistry
Background:
- Salidroside, derived from Rhodiola rosea, shows neuroprotection in transient stroke models.
- Its efficacy in permanent stroke models requires further investigation.
Purpose of the Study:
- To evaluate salidroside's neuroprotective effects in a permanent middle cerebral artery occlusion (pMCAO) rat model.
- To elucidate the underlying molecular mechanisms of salidroside's action.
Main Methods:
- Rats underwent permanent MCAO and received daily intraperitoneal injections of salidroside.
- Cerebral infarct volume, neurological deficit scores, and specific protein expressions (NeuN, Nrf2, HO-1, NFκB p50, IL-6, TNFα, p-PKB/PKB, C3, Egr1) were assessed.
- Inhibitors of Nrf2 (brusatol) and PI3K (LY294002) were used to probe signaling pathways.
Main Results:
- 100 mg/kg/day salidroside significantly reduced infarct volume and neurological deficits by day 7 post-pMCAO.
- Salidroside increased NeuN, Nrf2, HO-1, and p-PKB/PKB, while decreasing NFκB p50, IL-6, and TNFα.
- The PI3K/PKB/Nrf2/NFκB pathway mediated these effects, independent of complement C3.
Conclusions:
- Salidroside demonstrates significant neuroprotective effects in a pMCAO rat model.
- The mechanism involves the PI3K/PKB/Nrf2/NFκB signaling pathway, reducing neuroinflammation and neural damage.
- Salidroside's therapeutic potential for stroke warrants further study.
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