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Matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 expression in early focal cerebral infarction following urokinase thrombolysis in rats.

Song Y, Zou H, Wang G, Yang H, Xie Z, Bi J - Neural Regen Res (2012)

Bottom Line: A rat model of middle cerebral artery infarction was established by injecting autologous blood clots into the internal carotid artery.At 3 hours following model induction, urokinase was injected into the caudal vein.These results suggest that urokinase can suppress damage in the acute-early stage of cerebral infarction.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, the Affiliated Hospital of Medical College, Qingdao University, Qingdao 266003, Shandong Province, China.

ABSTRACT
Activity of matrix metalloproteinase-9 increases following cerebral ischemia/reperfusion, and is associated with cerebral microvascular permeability, blood-brain barrier destruction, inflammatory cell infiltration and brain edema. Matrix metalloproteinase-9 also likely participates in thrombolysis. A rat model of middle cerebral artery infarction was established by injecting autologous blood clots into the internal carotid artery. At 3 hours following model induction, urokinase was injected into the caudal vein. Decreased neurological severity score, reduced infarct volume, and increased expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 were observed in the cerebral cortex 24 hours after urokinase thrombolysis. These results suggest that urokinase can suppress damage in the acute-early stage of cerebral infarction.

No MeSH data available.


Related in: MedlinePlus

Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA expression in the cortex of rats with cerebral infarction (in situ hybridization, × 200).MMP-9 and TIMP-1 mRNA expression in the cortex was significantly greater in the urokinase group than in the model group. Arrows indicate positive expression. MMP-9 and TIMP-1 mRNA-positive cells exhibit a brown cytoplasm.
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Figure 3: Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA expression in the cortex of rats with cerebral infarction (in situ hybridization, × 200).MMP-9 and TIMP-1 mRNA expression in the cortex was significantly greater in the urokinase group than in the model group. Arrows indicate positive expression. MMP-9 and TIMP-1 mRNA-positive cells exhibit a brown cytoplasm.

Mentions: In situ hybridization showed MMP-9 and TIMP-1 mRNA expression in the cytoplasm of cells surrounding the infarct region in the model and urokinase groups. MMP-9 and TIMP-1 mRNA expression in the rat cortex was significantly greater in the urokinase group than in the model group (P < 0.01; Figure 3, Table 3).


Matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 expression in early focal cerebral infarction following urokinase thrombolysis in rats.

Song Y, Zou H, Wang G, Yang H, Xie Z, Bi J - Neural Regen Res (2012)

Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA expression in the cortex of rats with cerebral infarction (in situ hybridization, × 200).MMP-9 and TIMP-1 mRNA expression in the cortex was significantly greater in the urokinase group than in the model group. Arrows indicate positive expression. MMP-9 and TIMP-1 mRNA-positive cells exhibit a brown cytoplasm.
© Copyright Policy - open-access
Related In: Results  -  Collection

License
Show All Figures
getmorefigures.php?uid=PMC4308803&req=5

Figure 3: Matrix metalloproteinase-9 (MMP-9) and tissue inhibitor of metalloproteinase-1 (TIMP-1) mRNA expression in the cortex of rats with cerebral infarction (in situ hybridization, × 200).MMP-9 and TIMP-1 mRNA expression in the cortex was significantly greater in the urokinase group than in the model group. Arrows indicate positive expression. MMP-9 and TIMP-1 mRNA-positive cells exhibit a brown cytoplasm.
Mentions: In situ hybridization showed MMP-9 and TIMP-1 mRNA expression in the cytoplasm of cells surrounding the infarct region in the model and urokinase groups. MMP-9 and TIMP-1 mRNA expression in the rat cortex was significantly greater in the urokinase group than in the model group (P < 0.01; Figure 3, Table 3).

Bottom Line: A rat model of middle cerebral artery infarction was established by injecting autologous blood clots into the internal carotid artery.At 3 hours following model induction, urokinase was injected into the caudal vein.These results suggest that urokinase can suppress damage in the acute-early stage of cerebral infarction.

View Article: PubMed Central - PubMed

Affiliation: Department of Neurology, the Affiliated Hospital of Medical College, Qingdao University, Qingdao 266003, Shandong Province, China.

ABSTRACT
Activity of matrix metalloproteinase-9 increases following cerebral ischemia/reperfusion, and is associated with cerebral microvascular permeability, blood-brain barrier destruction, inflammatory cell infiltration and brain edema. Matrix metalloproteinase-9 also likely participates in thrombolysis. A rat model of middle cerebral artery infarction was established by injecting autologous blood clots into the internal carotid artery. At 3 hours following model induction, urokinase was injected into the caudal vein. Decreased neurological severity score, reduced infarct volume, and increased expression of matrix metalloproteinase-9 and tissue inhibitor of metalloproteinase-1 were observed in the cerebral cortex 24 hours after urokinase thrombolysis. These results suggest that urokinase can suppress damage in the acute-early stage of cerebral infarction.

No MeSH data available.


Related in: MedlinePlus