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Effect of low molecular weight heparin on the expression of endothelial protein C receptor and protease activated receptor 1 in abdominal aortic endothelial cells of septic rats / 中国医师杂志
Journal of Chinese Physician ; (12): 621-623, 2011.
Artículo en Chino | WPRIM | ID: wpr-416289
ABSTRACT
Objective To investigate the effect of low molecular weight heparin (LMWH) on the expression of endothelial protein C receptor (EPCR) and protease activated receptor 1 (PAR1) in abdominal vascular endothelial cells (VECs) of septic rats. Methods VECs were cultured by tissue-sticking method, and the purity was determined with flow cytometry (FCM). VECs were randomly divided into three groups control group, septic group (LPS 1 μg/ml) and LMWH group (LPS 1 μg/ml+LMWH 5 μg/ml). The VECs were collected at 1st, 3rd, 5th days after stimulated. The expression of EPCR and PAR1 were assessed by FCM. Results The expression of EPCR and PAR1 of septic group decreased significantly compared with control group at each time point (P<0.05 or P<0.01), and the expression decreased most obviously on day 5 (26.53±7.21 vs 39.26±2.62,q=6.45,P<0.01;53.21±15.10 vs 86.54±11.34,q=6.94,P<0.01). In LMWH group, the levels of EPCR and PAR1 expression were higher than setpic group at each time point (P<0.05). Compared to control group, the expression of EPCR had a significantly decrease on day 1 (40.86±1.63 vs 45.41±2.82,q=3.51,P<0.05), which had no significantly different on day 3 and 5 (41.20±3.32 vs 42.83±2.66,P>0.05;39.23±3.33 vs 39.26±2.62,P>0.05), and the expression of PAR1 were not significantly decrease compared with control group at each time point (P>0.05). Conclusions LMWH could improve the inhibition status and the expression of EPCR and PAR1 on VECs in septic rats.

Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Journal of Chinese Physician Año: 2011 Tipo del documento: Artículo

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Texto completo: Disponible Índice: WPRIM (Pacífico Occidental) Idioma: Chino Revista: Journal of Chinese Physician Año: 2011 Tipo del documento: Artículo