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Liu XR, Luo M, Yan F, et al. Ischemic postconditioning diminishes matrix metalloproteinase 9 expression and attenuates loss of the extracellular matrix proteins in rats following middle cerebral artery occlusion and reperfusion. CNS Neurosci Ther. 2012;18(10):855-63doi: 10.1111/j.1755-5949.2012.00366.x.
Liu, X. R., Luo, M., Yan, F., Zhang, C. C., Li, S. J., Zhao, H. P., Ji, X. M., & Luo, Y. M. (2012). Ischemic postconditioning diminishes matrix metalloproteinase 9 expression and attenuates loss of the extracellular matrix proteins in rats following middle cerebral artery occlusion and reperfusion. CNS neuroscience & therapeutics, 18(10), 855-63. https://doi.org/10.1111/j.1755-5949.2012.00366.x
Liu, Xiang-Rong, et al. "Ischemic postconditioning diminishes matrix metalloproteinase 9 expression and attenuates loss of the extracellular matrix proteins in rats following middle cerebral artery occlusion and reperfusion." CNS neuroscience & therapeutics vol. 18,10 (2012): 855-63. doi: https://doi.org/10.1111/j.1755-5949.2012.00366.x
Liu XR, Luo M, Yan F, Zhang CC, Li SJ, Zhao HP, Ji XM, Luo YM. Ischemic postconditioning diminishes matrix metalloproteinase 9 expression and attenuates loss of the extracellular matrix proteins in rats following middle cerebral artery occlusion and reperfusion. CNS Neurosci Ther. 2012 Oct;18(10):855-63. doi: 10.1111/j.1755-5949.2012.00366.x. Epub 2012 Aug 23. PMID: 22925005; PMCID: PMC6493466.
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CNS Neurosci Ther. 2012 Oct;18(10):855-63. doi: 10.1111/j.1755-5949.2012.00366.x. Epub 2012 Aug 23.

Ischemic postconditioning diminishes matrix metalloproteinase 9 expression and attenuates loss of the extracellular matrix proteins in rats following middle cerebral artery occlusion and reperfusion.

CNS neuroscience & therapeutics

Xiang-Rong Liu, Mei Luo, Feng Yan, Chen-Cheng Zhang, Si-Jie Li, Hai-Ping Zhao, Xun-Ming Ji, Yu-Min Luo

Affiliations

  1. Cerebrovascular Diseases Research Institute, Xuanwu Hospital of Capital Medical University, Key Laboratory of Neurodegenerative Diseases (Capital Medical University), Ministry of Education, Beijing, China.

PMID: 22925005 PMCID: PMC6493466 DOI: 10.1111/j.1755-5949.2012.00366.x

Abstract

AIMS: Ischemic postconditioning (IPostC) has been proved to have neuroprotective effects for cerebral ischemia, but the underlying mechanism remains elusive. This study aimed at validating the neuroprotective effects of IPostC and investigating whether the neuroprotection of IPostC is associated with matrix metalloproteinase 9 (MMP9) and the extracellular matrix proteins, laminin and fibronectin, following cerebral ischemia/reperfusion in rats.

METHODS: The rats in middle cerebral artery occlusion (MCAO) group underwent MCAO and reperfusion, and the animals in MCAO + IPostC group were treated by occluding bilateral common carotid arteries for 10 seconds and then reperfusing for 10 seconds for five episodes at the beginning of MCAO. Apoptosis was detected with terminal deoxynucleotidyl transferase dUTP nick end labeling staining. The expression of MMP9, laminin, and fibronectin was measured with immunofluorescence and enzyme-linked immunosorbent assay.

RESULTS: IPostC reduced brain edema and infarct volume and improved the neurological function. Furthermore, IPostC decreased cell apoptosis compared with the MCAO group. Compared to the MCAO group, IPostC treatment reduced MMP9 expression. Moreover, the results showed that the expression of laminin and fibronectin significantly increased in the MCAO + IPostC group compared to the MCAO group.

CONCLUSION: These findings indicated that diminishment of MMP9 expression and the attenuation of degradation of laminin and fibronectin may be involved in the protective mechanisms of postconditioning against cerebral ischemia/reperfusion injury.

© 2012 Blackwell Publishing Ltd.

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