Hydroxyethylpuerarin attenuates focal cerebral ischemia-reperfusion injury in rats by decreasing TNF-alpha expression and NF-kappaB activity.
- Author:
Hai-yan LOU
1
;
Xin-bing WEI
;
Bin ZHANG
;
Xia SUN
;
Xiu-mei ZHANG
Author Information
1. Institute of Pharmacology, School of Medicine, Shandong University, Jinan 250012, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Brain;
metabolism;
pathology;
Cytoplasm;
metabolism;
DNA;
metabolism;
I-kappa B Proteins;
metabolism;
Infarction, Middle Cerebral Artery;
complications;
Isoflavones;
pharmacology;
Male;
NF-KappaB Inhibitor alpha;
NF-kappa B;
metabolism;
Neuroprotective Agents;
pharmacology;
RNA, Messenger;
metabolism;
Rats;
Rats, Wistar;
Reperfusion Injury;
etiology;
metabolism;
pathology;
Tumor Necrosis Factor-alpha;
biosynthesis;
genetics
- From:
Acta Pharmaceutica Sinica
2007;42(7):710-715
- CountryChina
- Language:English
-
Abstract:
This study is to investigate the effect of hydroxyethylpuerarin on the expression of tumor necrosis factor-alpha (TNF-alpha) and activity of nuclear factor kappa B (NF-kappaB) after middle cerebral artery occlusion (MCAO) in rats. Rats were subjected to cerebral ischemia-reperfusion injury induced by MCAO. Hydroxyethylpuerarin (10, 20, 40 mg x kg(-1), iv) was administered just 30 min before occlusion and immediately after reperfusion. After a 24 h reperfusion following 2 h of MCAO, the number of viable neurons in hippocampal CA1 region was counted by hematoxylin and eosin (HE) staining. TNF-alpha protein and its mRNA expression were examined with radioimmunoassay (RIA) and reverse transcriptasepolymerase chain reaction (RT-PCR) respectively. NF-KB activity was observed by electrophoretic mobility shift assay (EMSA), and inhibition of NF-kappaB alpha (IkappaBalpha) protein expression was evaluated by Western blotting analysis. Animals treated with hydroxyethylpuerarin had a significant increase in neuronal survival in comparison with vehicle-treated group. Hydroxyethylpuerarin significantly reduced the protein and mRNA expression of TNF-alpha following 2 h of ischemia with 24 h of reperfusion. NF-kappaB DNA binding activity and the degradation of IkappaBalpha in the cytoplasm also decreased by hydroxyethylpuerarin treatment. The protective effects of hydroxyethylpuerarin against ischemia-reperfusion injury may be mediated by decreasing the expression of TNF-alpha and the activity of NF-kappaB in rats.
