Ischemic Postconditioning Diminishes Matrix Metalloproteinase 9 Expression and Attenuates Loss of the Extracellular Matrix Proteins in Rats Following Middle Cerebral Artery Occlusion and Reperfusion

Summary Aims Ischemic postconditioning ( IP ost C ) 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 IP ost C and investigating whether the neuroprotection of IP ost C is associated with matrix metalloproteinase 9 ( MMP 9) 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 + IP ost C 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 d UTP nick end labeling staining. The expression of MMP 9, laminin, and fibronectin was measured with immunofluorescence and enzyme‐linked immunosorbent assay. Results IP ost C reduced brain edema and infarct volume and improved the neurological function. Furthermore, IP ost C decreased cell apoptosis compared with the MCAO group. Compared to the MCAO group, IP ost C treatment reduced MMP 9 expression. Moreover, the results showed that the expression of laminin and fibronectin significantly increased in the MCAO + IP ost C group compared to the MCAO group. Conclusion These findings indicated that diminishment of MMP 9 expression and the attenuation of degradation of laminin and fibronectin may be involved in the protective mechanisms of postconditioning against cerebral ischemia/reperfusion injury.