Astragaloside IV attenuates cerebral ischemia and reperfusion injury and reduces activation of NLRP3 inflammasome and NF-κB phosphorylation in rats following a transient middle cerebral artery occlusion.
- Author:
Biao TANG
1
;
Wen-Jing TANG
1
;
Ying-Hong TANG
1
;
Chang-Qing DENG
2
Author Information
1. Medical School, Hunan University of Chinese Medicine, Changsha 410028, China.
2. Medical School, Hunan University of Chinese Medicine, Changsha 410028, China. dchangq@sohu.com.
- Publication Type:Journal Article
- MeSH:
Animals;
Brain Ischemia;
drug therapy;
Infarction, Middle Cerebral Artery;
drug therapy;
Inflammasomes;
metabolism;
NF-kappa B;
metabolism;
NLR Family, Pyrin Domain-Containing 3 Protein;
metabolism;
Phosphorylation;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury;
drug therapy;
Saponins;
pharmacology;
Triterpenes;
pharmacology
- From:
Acta Physiologica Sinica
2019;71(3):424-430
- CountryChina
- Language:Chinese
-
Abstract:
The present study was aimed to investigate the protective effect and anti-inflammation mechanism of astragaloside IV (AST-IV) on cerebral ischemia and reperfusion injury. Following the establishment of cerebral ischemia and reperfusion model in rats by modified suture method, neurological deficit scores and cerebral infarct volume were used to evaluate the pharmacological effect of AST-IV against cerebral ischemia-reperfusion injury. Western blot was used to detect the expression levels of NLRP3, pro-Caspase-1, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18, IL-18, phosphorylated and total nuclear factor kappa B (NF-κB)/p65 protein in the brain tissue. The results showed that compared with model group, the intervention of AST-IV decreased the neurological deficit scores, reduced the cerebral infarct volume, decreased the levels of NLRP3, Caspase-1, pro-IL-1β, IL-1β, pro-IL-18 and IL-18, and inhibited the expression of phosphorylated NF-κB in brain tissue. The results suggest that AST-IV has a protective effect against cerebral ischemia and reperfusion injury, and its mechanism is related to inhibiting the phosphorylation of NF-κB and NLRP3 inflammasome activation.
