Chlorogenic acid ameliorates brain damage and edema by inhibiting matrix metalloproteinase-2 and 9 in a rat model of focal cerebral ischemia

2012 ◽  
Vol 689 (1-3) ◽  
pp. 89-95 ◽  
Author(s):  
Kyungjin Lee ◽  
Jeong-Sook Lee ◽  
Hyeung-Jin Jang ◽  
Sung-Moo Kim ◽  
Mun Seog Chang ◽  
...  
2012 ◽  
Vol 1450 ◽  
pp. 116-124 ◽  
Author(s):  
Zhen Li ◽  
Liang Pang ◽  
Fang Fang ◽  
Gongliang Zhang ◽  
Jin Zhang ◽  
...  

1999 ◽  
Vol 19 (6) ◽  
pp. 624-633 ◽  
Author(s):  
Ji Hoe Heo ◽  
Jacinta Lucero ◽  
Takeo Abumiya ◽  
James A. Koziol ◽  
Brian R. Copeland ◽  
...  

Microvascular integrity is lost during focal cerebral ischemia. The degradation of the basal lamina and extracellular matrix are, in part, responsible for the loss of vascular integrity. Matrix metalloproteinases (MMPs) may play a primary role in basal lamina degradation. By using a sensitive modification of gelatin zymography, the authors investigated the activity of MMP-2 and MMP-9 in frozen 10-µm sections of ischemic and nonischemic basal ganglia and plasma samples of 27 non-human primates after middle cerebral artery occlusion/reperfusion (MCAO/R) for various periods. The gelatinolytic activities were compared with parallel cell dUTP incorporation in the ischemic zones of adjacent sections. In the brain, the integrated density of MMP-2 increased significantly by 1 hour after MCAO and was persistently elevated thereafter. Matrix metalloproteinase-2 expression was highly correlated with the extent of neuron injury and the number of injured neurons (r = 0.9763, SE = 0.004, 2 P < 0.0008). Matrix metalloproteinase-9 expression only was significantly increased in subjects with hemorrhagic transformation. In plasma, only MMP-9 increased transiently at 2 hours of MCAO. These findings highlight the early potential role of MMP-2 in the degradation of basal lamina leading to neuronal injury, and an association of MMP-9 with hemorrhagic transformation after focal cerebral ischemia.


2015 ◽  
Vol 5 (1) ◽  
Author(s):  
Bharath Chelluboina ◽  
Aditi Warhekar ◽  
Matt Dillard ◽  
Jeffrey D. Klopfenstein ◽  
David M. Pinson ◽  
...  

2005 ◽  
Vol 25 (1_suppl) ◽  
pp. S94-S94
Author(s):  
Kudret Tureyen ◽  
Ramya Sundaresan ◽  
Kellie Bowen ◽  
Raghu Vemuganti

2011 ◽  
Vol 2011 ◽  
pp. 1-8 ◽  
Author(s):  
Jintanaporn Wattanathorn ◽  
Jinatta Jittiwat ◽  
Terdthai Tongun ◽  
Supaporn Muchimapura ◽  
Kornkanok Ingkaninan

Cerebral ischemia is known to produce brain damage and related behavioral deficits including memory. Recently, accumulating lines of evidence showed that dietary enrichment with nutritional antioxidants could reduce brain damage and improve cognitive function. In this study, possible protective effect ofZingiber officinale, a medicinal plant reputed for neuroprotective effect against oxidative stress-related brain damage, on brain damage and memory deficit induced by focal cerebral ischemia was elucidated. Male adult Wistar rats were administrated an alcoholic extract of ginger rhizome orally 14 days before and 21 days after the permanent occlusion of right middle cerebral artery (MCAO). Cognitive function assessment was performed at 7, 14, and 21 days after MCAO using the Morris water maze test. The brain infarct volume and density of neurons in hippocampus were also determined. Furthermore, the level of malondialdehyde (MDA), superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) in cerebral cortex, striatum, and hippocampus was also quantified at the end of experiment. The results showed that cognitive function and neurons density in hippocampus of rats receiving ginger rhizome extract were improved while the brain infarct volume was decreased. The cognitive enhancing effect and neuroprotective effect occurred partly via the antioxidant activity of the extract. In conclusion, our study demonstrated the beneficial effect of ginger rhizome to protect against focal cerebral ischemia.


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