The effect of zinc on inflammatory reaction in rats with focal cerebral ischemia/reperfusion
10.16438/j.0513-4870.2015-1066
- VernacularTitle:锌离子对大鼠局灶性脑缺血再灌注损伤模型中炎性反应的影响
- Author:
Ting LIU
1
;
Dan-qing SONG
1
;
Lu-yong ZHANG
2
;
Pei-li HU
2
;
Shi-bu LIU
2
;
Wei ZUO
3
Author Information
1. Institute of Medicinal Biotechnology, Chinese Academy of Medical Sciences and Peking Union Medical College, Beijing 100050, China
2. National Institutes for Food and Drug Control, Beijing 100050, China
3. Peking Union Medical College Hospital, Chinese Academy of Medical Sciences, Beijing 100730, China
- Publication Type:ORIGINAL ARTICLES
- Keywords:
zinc;
middle cerebral artery occlusion;
N, N-diethyldithiocarbamate;
inflammatory cytokine
- From:
Acta Pharmaceutica Sinica
2016;51(6):892-
- CountryChina
- Language:Chinese
-
Abstract:
This study was conducted to investigate the effect of N, N-diethyldithiocarbamate (DEDTC) on the changes of inflammatory cytokines after focal cerebral ischemia-reperfusion injury in rats and to explore the potential mechanism. Two hundred Sprague Dawley male rats were randomly divided into sham group, middle cerebral artery occlusion (MCAO) group and DEDTC (Zn chelator) treated group. MCAO model was established by the suture method. Rats were sacrificed at 6, 12 and 24 h after reperfusion. 2, 3, 5-Triphenyltetrazolium chloride (TTC) was conducted to measure the brain infarct volume. Newport Green was adopted to detect the chelatable zinc in the cerebral penumbra. Enzyme linked immunosorbent assay (ELISA) was performed to determine the release of TNF-α and IL-6. Furthermore Western blot was used to analyze the expression of the PI3K/Akt/NF-κB signaling pathway. The results showed that DEDTC resulted in a significant reduction of brain infarct volume and an obvious improvement of neurological function compared to the model group. DEDTC also decreased the release of inflammatory cytokines such as TNF-α and IL-6. The activation of PI3K/Akt/NF-κB signaling pathway induced by I/R injury was drastically inhibited by the treatment with DEDTC. In conclusion, DEDTC could protect the brain against ischemic injury induced by MCAO, which might be relevant to the inhibition of PI3K/Akt/NF-κB signaling pathway, and the decreased release of inflammatory cytokines.
