Potential role of soluble biglycan induces the production of ICAM-1 following spinal I/R injury through ERK1/2 pathway

doi: 10.18081/ajbm/2333-5106/015-04/171-180    
American Journal of BioMedicine Volume 3, Issue 4, pages 171-180 April 2014
Published: April 11, 2015

Musaed Hekmat Aldhhan


The elusive mechanism of spinal cord ischemia-reperfusion injury has delayed the development of pharmacological adjuncts. The objective of this study is to investigate the neuroprotective role of biglycan in spinal injury following I/R after aortic occlusion via down-regulation of ICAM-1 involving ERK1/2 pathway. Adult male Albino rats were underwent aortic occlusion for 5 minutes, followed by 48 hours of reperfusion when spinal cords were removed for analysis. Rat treated with biglycan attenuated ICAM-1 expression with down-regulation of ERK1/2 pathway. Further; biglycan decreased cytokine production and had preserved functional outcomes and neuronal viability after thoracic aortic occlusion. In conclusion, biglycan attenuated neuronal injury after thoracic aortic occlusion in rat through decreased the activity of ERK1/2 pathway that significantly attenuated the production of proinflammatory cytokines.

Keywords: Biglycan; ICAM-1; ERK1/2; Spinal cord I/R  

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