چکیده (انگلیسی):

Objective: To discuss the expression and significance of angiostatin, vascular endothelial
growth factor and matrix metalloproteinase-9 in the brain tissue of diabetic rats
with ischemia reperfusion.
Methods: A total of 60 male Wistar rats were randomly divided into the normal group,
sham group, diabetic cerebral infarction group and single cerebral infarction group according
to the random number table, with 15 rats in each group. The high sucrose diet and
intraperitoneal injection of streptozotocin were performed for the modeling of diabetic
rats, while the thread-occlusion method was employed to build the model of cerebral
ischemia reperfusion. The immunohistochemical staining was performed to detect the
expression of angiostatin, vascular endothelial growth factor (VEGF) and matrix
metalloproteinase-9 (MMP-9) in the brain tissue.
Results: The expression of angiostatin after the reperfusion in the brain tissue of rats in
the single cerebral infarction group and diabetic cerebral infarction group was increased
6 h after the reperfusion, reached to the peak on 1 d and then decreased gradually. The
expression of angiostatin in the diabetic cerebral infarction group 6 h, 1 d, 3 d and 7 d
after the reperfusion was significantly higher than that in the single cerebral infarction
group (P < 0.05). VEGF began to be increased 1 h after the reperfusion in the single
cerebral infarction group and diabetic cerebral infarction group, reached to the peak at 6 h
and then decreased gradually. The expression of VEGF in the diabetic cerebral infarction
group at each time point after the reperfusion was significantly lower than that in the
single cerebral infarction group (P < 0.05). MMP-9 began to be increased 1 h after the
reperfusion in the single cerebral infarction group and diabetic cerebral infarction group,
reached to the peak on 1 d and then decreased gradually. The expression of MMP-9 in the
diabetic cerebral infarction group at each time point after the reperfusion was significantly
higher than that in the single cerebral infarction group (P < 0.05).
Conclusions: The high glucose environment in which the diabetic cerebral infarction is
occurred is to induce the formation of MMP-9 at first and then activate and increase the
expression of angiostatin. Afterwards, the expression of VEGF is inhibited, resulting in
the poor angiogenesis after cerebral infarction, which thus makes the injury of brain tissue
after cerebral infarction even worse than the non-diabetes mellitus.