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1.
Journal of Jilin University(Medicine Edition) ; (6): 1137-1141,后插1, 2017.
Article in Chinese | WPRIM | ID: wpr-668081

ABSTRACT

Objective:To investigate the effect of alteplase on the expressions of Claudin-1 and Claudin-5 proteins in the vascular endothelial cells after thrombolysis in the rats with acute cerebral infarction and its mechanism,and to provide experimental evidence for its clinical application. Methods: The models of acute thrombosis of middle cerebral artery of the rats were established.Fifty-four SD rats were randomly divided into sham operation group,model group and alteplase group (n= 18).The ultrastructure of brain endothelial cells of the rats was observed under transmission electron microscope.The expression levels of Claudin-1 and Claudin-5 proteins in the vascular endothelial cells of the rats were detected by immunoflurorescence and Western blotting methods.Results:The transmission electron microscope results showed that the brain volume in the ischemic area of the rats in model group was significantly increased and the endothelial cells were swollen,some of the cortical and surrounding brain tissues had obvious boundaries,and the thickness of the basement membrane was uniform and the tightly connected structure was very loose and disappeared;the swelling condition of the capillary endothelial cells in infarcted area of the rats in alteplase group was significantly reduced and the thickness of the basement membrane was improved,and most of the tightly connected structures between the brain capillary endothelial cells and the endothelial cells were loose and the fracture was lost and the structure disappeared.The immunofluorescence results showed that the expressions of Claudin-1 and Claudin-5 proteins in the vascular endothelial cells of the rats in alteplase group were significantly improved compared with model group. The Western blotting results showed the expression levels of Claudin-1 and Claudin-5 proteins in the vascular endothelial cells of the rats in model group were significantly decreased compared with sham operation group (P < 0.01 ); compared with model group, the expression levels of Claudin-1 and Claudin-5 proteins in the vascular endothelial cells of the rats in alteplase group at different time points were increased (P < 0.01 ). Conclusion: Alteplase can improve the structure of brain endothelial cells in the rats with acute cerebral infarction,and the mechanism may be related to decreasing the expressions of Claudin-1 and Claudin-5 proteins in the vascular endothelial cells of the rats induced by alteplase.

2.
International Journal of Traditional Chinese Medicine ; (6): 111-113, 2011.
Article in Chinese | WPRIM | ID: wpr-414627

ABSTRACT

Objective To investigate the vasodilatation effects of total flavonoid from polygonum aviculare on rat thoracic aorta and its underlying mechanisms. Methods Total flavonoid from polygonum aviculare was gotten by extracted with 65% alcohol, gathered with polyamide, and eluted with 75% alcohol.The content of flavone was determined with rutoside as standard preparation. Normal rats thoracic aorta in vitro used as sample, BL-420E biological functional experiment system was utilized to record dilatation effect of total flavonoid on PE affecting pre-contracting blood vessel and the relation between dilatation effect of total flavonoid on blood vessel and calcium influx. Results Total flavonoids from polygonum aviculare can diastole contractions of thoracic aorta caused by PE. In calcium-free perfusion, gradually adding CaCl2 induced calcium influx. Clinical data showed dose-effect relation between drug and blood vessel contraction decreased in the total flavonoids from polygonum aviculare incubation rats than normal rats. Besides, total flavonoids from polygonum aviculare can obviously inhibit contraction of blood vascular circle induced by calcium releasing.Conclusion FP exerted a dose-dependent vasodilatation effect on rat isolated aorta rings by inhibiting Ca2+influx via L-type voltage-gated Ca2+ channels and Ca2+ release from sarcoplasmic reticulum, consequently decrease Ca2+ in vascular smooth muscle cells.

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