Mechanism of the reduction of cerebral ischemic-reperfusion injury through inhibiting the activity of NF-kappaB by propyl gallate.
- Author:
Jian-ming ZHENG
1
;
Xiao-chun CHEN
;
Min LIN
;
Jing ZHANG
;
Zhi-ying LIN
;
Guan-yi ZHENG
;
Kang-zeng LI
Author Information
1. Department of Neurology, the Affiliated Union Hospital of Fujian Medical University, Fuzhou 350001, China.
- Publication Type:Journal Article
- MeSH:
Animals;
Cyclooxygenase 2;
metabolism;
HSP70 Heat-Shock Proteins;
metabolism;
Infarction, Middle Cerebral Artery;
complications;
Male;
Propyl Gallate;
pharmacology;
RNA, Messenger;
metabolism;
Random Allocation;
Rats;
Rats, Sprague-Dawley;
Reperfusion Injury;
etiology;
metabolism;
Toll-Like Receptor 4;
genetics;
metabolism;
Transcription Factor RelA;
metabolism;
Tumor Necrosis Factor-alpha;
metabolism
- From:
Acta Pharmaceutica Sinica
2011;46(2):158-164
- CountryChina
- Language:Chinese
-
Abstract:
The probable mechanism of the reduction of rat cerebral ischemic-reperfusion injury by propyl gallate was studied. Intraluminal suture middle cerebral artery occlusion model of rat was employed. Propyl gallate was injected immediately after the ischemia was happened. The activity of NF-kappaB, and the expression of COX-2 and HSP70 on the peripheral ischemia were determined by Western blotting. The expression of TNF-alpha was determined by ELISA assay. RT-PCR and immunofluorescence staining were employed to detect the transcription and expression of TLR-4. Results showed that propyl gallate could inhibit the activity of NF-kappaB in the peripheral ischemia, and reduce the expression of COX-2 and TNF-alpha. As the upstream of NF-kappaB, the transcription and expression of TLR-4 decreased, as well as HSP70, the endogenic ligand of TLR-4. As an antioxidant, propyl gallate could reduce the cerebral ischemic-reperfusion injury through inhibiting the activity of NF-kappaB and decreasing the COX-2 and TNF-alpha in the peripheral ischemia. It also could influence HSP70 and TLR-4.
