Protective Effect and Mechanism of Sodium Ferulate on Cerebral Ischemia-reperfusion Inflammatory Injury in Rats
10.13422/j.cnki.syfjx.20190341
- VernacularTitle: 阿魏酸钠对大鼠脑缺血再灌注炎症损伤的保护作用及机制分析
- Author:
Wan GONG
1
;
Xiao-ling CHEN
1
;
Li ZHOU
2
;
Ke-na ZHANG
1
Author Information
1. College of Basic Medical Science, Zhejiang Chinese Medical University, Hangzhou 310053, China
2. The First Affiliated Hospital of Zhejiang Chinese Medical University, Hangzhou 310006, China
- Publication Type:Research Article
- Keywords:
sodium ferulate;
cerebral ischemia reperfusion;
tumor necrosis factor-α(TNF-α);
interleukin-1β(IL-1β);
interleukin-6(IL-6);
nuclear factor-kappa B (NF-κB)
- From:
Chinese Journal of Experimental Traditional Medical Formulae
2019;25(3):94-99
- CountryChina
- Language:Chinese
-
Abstract:
Objective: To investigate the protective effect of sodium ferulate on cerebral ischemia-reperfusion injury in rats and to explore its possible mechanism.Method: The cerebral ischemia reperfusion injury model was established by middle cerebral artery occlusion (MCAO) in SD male rats. 36 modeled rats with neurologic damage were randomly divided into 4 groups:model group, low,medium,high-dose sodium ferulate groups (25,50,100 mg·kg-1).Another nine rats were selected as a sham operation group.Neurological function was assessed by neurological scoring system in rats.Hematoxylin-eosin (HE) staining was performed to observe the pathological changes of the rats' brain. The levels of tumor necrosis factor α (TNF-α), interleukin-1β (IL-1β) and interleukin-6 (IL-6) in serum and brain tissues were detected by enzyme-linked immunosorbent assay (ELISA). Western blot was used to detect the protein expression of nucleus and cytoplasm nuclear factor-kappa B p65 (NF-κB p65) in brain tissues.Result: As compared with normal group, neurological deficit score was increased; the neuronal necrosis and inflammatory cell number were present;the serum and brain tissue levels of TNF-α, IL-1β and IL-6 were increased; nucleus/cytoplasm NF-κB p65 protein expression ratio was increased significantly in model group (P<0.01).As compared with model group, sodium ferulate distinctly decreased the neurological deficit score(P<0.05, P<0.01), inhibited neuronal necrosis, reduce inflammatory cell number, significantly reduce the serum and brain tissue levels of TNF-α, IL-1β and IL-6(P<0.05, P<0.01).Western blot showed that sodium ferulate could inhibit the nuclear translocation of NF-κB p65 protein(P<0.05, P<0.01), and finally, it can alleviate the inflammatory injury caused by ischemia reperfusion.Conclusion: Sodium ferulate protects the brain against focal cerebral ischemia reperfusion injury, and the mechanism may be related to inhibiting nuclear translocation of NF-κB p65 protein to alleviate inflammatory response.
