Matrix metalloproteinase-9 potentiates early brain injury after subarachnoid hemorrhage

Abstract

MMP-9 may be involved in early brain injury through degradation of laminin and neuronal death, and inhibition of MMP-9 may be a potential direction for brain protection after SAH.

Peroxisome Proliferator–Activated Receptor β/δ Alleviates Early Brain Injury After Subarachnoid Hemorrhage in Rats

“…13,15 In the present work, the overexpression of PPARβ/δ resulted in reduction of neuronal apoptosis and alleviation of BBB damage, which is directly associated with downregulation of MMP-9 activity.…”

“…The procedures were according to the protocol of the kit and our previous study. 13 Briefly, the sections were dewaxed in xylene and treated by 1% Triton X-100 for 10 minutes. Then they were incubated in newly prepared TUNEL reaction solution at 37°C for 1 hour and peroxidase (POD) solution at 37°C for 30 minutes.…”

“…But in pathological condition, MMP-9 can especially attack type IV collagen, laminin, and fibronectin, the major components of the basal lamina. 12 In our previous study, [13][14][15] the expression of MMP-9 was found increased greatly with laminin reduced and apoptosis increased at 24 hours after SAH in rats, whereas laminin degradation and neuronal death could be alleviated by inhibiting MMP-9 after SAH. In addition, it is indicated that MMP-9 could be downregulated by NF-κB suppression.…”

Selective Gelatinase Inhibitor Neuroprotective Agents Cross the Blood-Brain Barrier

“…This compound has shown efficacy in a number of neurological diseases, including blocking laminin degradation by MMP-9 and rescuing neurons from apoptosis after transient focal cerebral ischemia, 2 preventing laminin degradation after subarachnoid hemorrhage, 3 reducing cerebral vasopasm caused by subarachnoid hemorrhage, 4 reducing the infiltration of monocytes into the injured spinal cord, 5 and decreasing extravasation and apoptotic cell death after spinal cord injury. 6 The compounds of the thiirane class have a unique mechanism of action, involving ring-opening of the thiirane ring at the active site of gelatinases and generation of the thiolate, which is a picomolar and tight-binding inhibitor.…”

Astaxanthin reduces matrix metalloproteinase-9 expression and activity in the brain after experimental subarachnoid hemorrhage in rats

“…Once neurovascular barriers are affected, there is a resultant activated of multiple neuro-inflammatory cascades, which could further increase the MMP-9 expression and activity, leading to much more damage to the BBB (Morancho et al, 2010). There is a considerable of evidence indicating that MMP-9 is up-regulated after the onset of SAH insults, associated with the disruption of BBB permeability and the formation of vasogenic edema (Feiler et al, 2011;Guo et al, 2010a;Guo et al, 2010b;Sozen et al, 2009;Suzuki et al, 2010). In addition, activation of MMP-9 could lead to cell death via degradation of the microvessel basal lamina protein laminin, a main component of ECM, after SAH (Gu et al, 2005;Guo et al, 2010b).…”