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JOURNAL ARTICLE
RESEARCH SUPPORT, NON-U.S. GOV'T
Ischemic preconditioning protects against myocardial ischemia-reperfusion injury through inhibiting toll-like receptor 4/NF-κB signaling pathway in rats.
Zhong Nan da Xue Xue Bao. Yi Xue Ban = Journal of Central South University. Medical Sciences 2011 October
OBJECTIVE: To investigate whether the protection of ischemic preconditioning (IPC) against myocardial ischemia/reperfusion (I/R) injury is mediated by toll-like receptor 4 (TLR4)/NF-κB pathway,and whether these effects are related to the release of calcitonin gene-related peptide (CGRP).
METHODS: Sprague-Dawley rats were subjected to 60 min of ligation of the left anterior descending coronary artery followed by 3 h of reperfusion to induce I/R injury. IPC was performed by 4 cycles of 3-min left coronary artery occlusion followed by 5-min reperfusion before the I/R. The expression of TLR4 mRNA was determined by RT-PCR. TLR4 and NF-κB protein expression were analyzed by immunohistochemistry. Myocardial infarct size,CGRP concentration in plasma and activity of creatine kinase in serum were also measured.
RESULTS: IPC significantly reduced the infarct size and creatine kinase activity concomitantly with the increase in plasma CGRP concentration. The expressions of TLR4 protein and mRNA and NF-κB protein were increased by myocardial I/R injury,and dramatically inhibited by IPC.
CONCLUSION: IPC protects against myocardial I/R injury by inhibition of TLR4/NF-κB pathway. These effects are related to the increased the release of CGRP.
METHODS: Sprague-Dawley rats were subjected to 60 min of ligation of the left anterior descending coronary artery followed by 3 h of reperfusion to induce I/R injury. IPC was performed by 4 cycles of 3-min left coronary artery occlusion followed by 5-min reperfusion before the I/R. The expression of TLR4 mRNA was determined by RT-PCR. TLR4 and NF-κB protein expression were analyzed by immunohistochemistry. Myocardial infarct size,CGRP concentration in plasma and activity of creatine kinase in serum were also measured.
RESULTS: IPC significantly reduced the infarct size and creatine kinase activity concomitantly with the increase in plasma CGRP concentration. The expressions of TLR4 protein and mRNA and NF-κB protein were increased by myocardial I/R injury,and dramatically inhibited by IPC.
CONCLUSION: IPC protects against myocardial I/R injury by inhibition of TLR4/NF-κB pathway. These effects are related to the increased the release of CGRP.
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