Infarct volume was quantified at 48 h. Data showed that BET degradation significantly reduced infarct volume in permanent focal cerebral ischemia in aged mice, and this was associated with reduced brain levels of pro-inflammatory mediators including TNF-α, CXCL1, CXCL10, CCL2, and matrix metalloproteinase-9.
These results demonstrate that absence of MCPIP1 exacerbates cerebral I/R-induced BBB disruption by enhancing the expression of MMP-9/3 and the degradation of claudin-5 and ZO-1, providing novel insights into the mechanisms underlying BBB breakdown after cerebral ischemia/reperfusion.
The expressions of vascular endothelial growth factor (VEGF) and matrix metalloproteinase 9 (MMP-9) were supposed to show the changing circumstances for neural generation under cerebral ischemia.
The mRNA expressions of MMP-2 and MMP-9 in AMI-CI group were also significantly higher than those in the AMI group, and the differences between the two groups were statistically significant (p<0.05).
Our results suggested that SAA could be a promising agent to attenuate cerebral ischemia reperfusion injury through MMP-9 inhibition and anti-inflammation activities.
<b>Objective:</b> To determine the neuroprotective effects and underpinning mechanisms of thrombopoietin (TPO), Matrix Metalloproteinase-9(MMP-9) and Nuclear Factor-κB (NF-κB) after focal cerebral ischemia-reperfusion in rats.
The larger the carotid IMT is, the more unstable the plaque is and the higher the levels of serum inflammatory factors, MMP-2 and MMP-9 are, the greater the risk of acute cerebral infarction will be.
A functional polymorphism at miR-491-5p binding site in the 3'-UTR of MMP-9 gene confers increased risk for atherosclerotic cerebral infarction in a Chinese population.
Serum levels of soluble OX40L and matrix metalloproteinase 9 levels were significantly reduced in patients with atherosclerotic cerebral infarction who were treated for 6 months with routine therapy plus simvastatin (n = 46) compared with patients receiving routine therapy alone (n = 30).
The matrix-degrading metalloproteinases (MMPs), particularly MMP-9, are involved in the neuroinflammation processes leading to disrupting of the blood brain barrier (BBB), thereby exacerbating neurological diseases such as HIV-1 AIDS dementia and cerebral ischemia.
Oxidative stress is also implicated in the pathogenesis after cerebral ischemia and spinal cord injury (SCI), but the relationship between MMP-9 activation and oxidative stress after SCI has not yet been clarified.
Influence of hyperglycemia on oxidative stress and matrix metalloproteinase-9 activation after focal cerebral ischemia/reperfusion in rats: relation to blood-brain barrier dysfunction.
Although MMP-9 level predicts PH appearance after tPA treatment, no relationship exists with the C-1562T polymorphism, probably because this mutation is not functional in response to cerebral ischemia in vivo.
In this study we demonstrate that an increase in endogenous tissue-type plasminogen activator (tPA) activity in the perivascular tissue following cerebral ischemia induces opening of the BBB via a mechanism that is independent of both plasminogen (Plg) and MMP-9.