The cardioprotective effect of fluvastatin on ischemic injury via down-regulation of toll-like receptor 4 |
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Authors: | Jun Yang Xiao-Dong Zhang Jian Yang Jia-Wang Ding Zhao-Qi Liu Shu-Guo Li Rui Yang |
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Institution: | (1) Department of Cardiology, The First College of Clinical Medical Sciences, China Three Gorges University, 443000 Yichang, Hubei Province, China;(2) Department of Cardiology, Yichang Central People’s Hospital, 443000 Yichang, Hubei Province, China;(3) The Institute of Molecular Biology, China Three Gorges University, 443000 Yichang, Hubei Province, China;(4) Tongji Medical College of Huazhong University of Science and Technology, 430000 Wuhan, Hubei Province, China; |
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Abstract: | To determine whether the cardioprotection effect of fluvastatin mediates by toll-like receptor 4 (TLR4) signaling pathway,
fifty Sprague–Dawley rats were randomly divided into five groups: sham operation group, ischemia/reperfusion (I/R) group,
fluvastatin groups (high-dosage, medium-dosage, low-dosage, n = 10 in each group). Except sham operation group, the rest four groups of rats were artificially afflicted with coronary
occlusion for 30 min, then reperfusion 2 h. Light microscope and transmission electronic microscope were used to observe structural
changes of myocardium. RT–PCR was used to measure TLR4 mRNA expression level, TLR4 protein expression was detected by immunohistochemistry.
Western blot was used to measure myocardial NF-κB protein level; ELISA was used to measure the level of TNF-α in myocardium.
The results demonstrated that fluvastatin treatment markedly decreased ischemic injury caused by ischemia/reperfusion, and
inhibited the expression levels of TLR4, TNF-α and NF-κB, all of which up-regulated by ischemia/reperfusion. Taken together,
our results suggest that proper dosage of fluvastatin may have protective effect on the ischemic injury mediated by ischemia/reperfusion
in the hearts, which might be associated with inhibition of TLR4 signaling pathway and inflammatory response during ischemia/reperfusion. |
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