OBJECTIVE: To investigate the effects of Propyl Gallate (PrG) on cellular adhesion between human To investigate the effects of Propyl Gallate (PrG) on cellular adhesion between human umbilical vein endothelial cells (HUVEC) and polymorphonuclear leukocytes (PMN) as well as the expression umbilical vein endothelial cells (HUVEC) and polymorphonuclear leukocytes (PMN) as well as the expression of intercellular adhesion molecule-1 (ICAM-1, CD54) and E-selectin (CD62E) on the VEC surface. of intercellular adhesion molecule-1 (ICAM-1, CD54) and E-selectin (CD62E) on the VEC surface. METHODS: A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-alpha). VECs were pre- A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-alpha). VECs were preincubated with varying concentrations of PrG (0.001-5 mmol/L) or 1 per thousand DMSO (v:v) or 10 mmol/L acetylsalicylic incubated with varying concentrations of PrG (0.001-5 mmol/L) or 1 per thousand DMSO (v:v) or 10 mmol/L acetylsalicylic acid (ASA) for 1 h, and then were stimulated with 10 ng/mL TNF-alpha for 6 h. Rose bengal vital staining method acid (ASA) for 1 h, and then were stimulated with 10 ng/mL TNF-alpha for 6 h. Rose bengal vital staining method was used to measure the adherence rate of PMN to VEC, while flow cytometry was used to determine the was used to measure the adherence rate of PMN to VEC, while flow cytometry was used to determine the expression of CD54 and CD62E on the VEC surface. expression of CD54 and CD62E on the VEC surface. RESULTS: After 6 h of incubation with TNF-alpha, the adherence After 6 h of incubation with TNF-alpha, the adherence of PMN to HUVECs as well as the percentage of fluorescence-positive cells and mean fluorescence intensity of PMN to HUVECs as well as the percentage of fluorescence-positive cells and mean fluorescence intensity (MFI) of surface CD54 and CD62E in HUVECs increased significantly ( (MFI) of surface CD54 and CD62E in HUVECs increased significantly (P<0.01). Pre-treatment of HUVECs with <0.01). Pre-treatment of HUVECs with PrG (0.1-5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-alpha (PrG (0.1-5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-alpha (P<0.05). PrG <0.05). PrG (1-5 mmol/L) inhibited the VEC surface expression of CD62E and CD54 in a dose-dependent way ( (1-5 mmol/L) inhibited the VEC surface expression of CD62E and CD54 in a dose-dependent way (P<0.05). PrG <0.05). PrG at lower concentrations (0.001-0.1 mmol/L) showed no effect on CD54 expression, while it showed a slightly at lower concentrations (0.001-0.1 mmol/L) showed no effect on CD54 expression, while it showed a slightly increasing trend in CD62E expression (increasing trend in CD62E expression (P>0.05). ASA at 10 mmol/L had no obvious effect on the positive rate of >0.05). ASA at 10 mmol/L had no obvious effect on the positive rate of CD62E and CD54. CD62E and CD54. CONCLUSIONS: High concentrations of PrG (0.1-5 mmol/L) exert its inhibitory effect on cellular High concentrations of PrG (0.1-5 mmol/L) exert its inhibitory effect on cellular adherence of PMN to HUVECs, and its mechanism may be related to inhibiting surface expression of CD54 and adherence of PMN to HUVECs, and its mechanism may be related to inhibiting surface expression of CD54 and CD62E in HUVECs. Its action concentration was lower than that of ASA. CD62E in HUVECs. Its action concentration was lower than that of ASA.
OBJECTIVE: To investigate the effects of Propyl Gallate (PrG) on cellular adhesion between human To investigate the effects of Propyl Gallate (PrG) on cellular adhesion between human umbilical vein endothelial cells (HUVEC) and polymorphonuclear leukocytes (PMN) as well as the expression umbilical vein endothelial cells (HUVEC) and polymorphonuclear leukocytes (PMN) as well as the expression of intercellular adhesion molecule-1 (ICAM-1, CD54) and E-selectin (CD62E) on the VEC surface. of intercellular adhesion molecule-1 (ICAM-1, CD54) and E-selectin (CD62E) on the VEC surface. METHODS: A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-alpha). VECs were pre- A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-alpha). VECs were preincubated with varying concentrations of PrG (0.001-5 mmol/L) or 1 per thousand DMSO (v:v) or 10 mmol/L acetylsalicylic incubated with varying concentrations of PrG (0.001-5 mmol/L) or 1 per thousand DMSO (v:v) or 10 mmol/L acetylsalicylic acid (ASA) for 1 h, and then were stimulated with 10 ng/mL TNF-alpha for 6 h. Rose bengal vital staining method acid (ASA) for 1 h, and then were stimulated with 10 ng/mL TNF-alpha for 6 h. Rose bengal vital staining method was used to measure the adherence rate of PMN to VEC, while flow cytometry was used to determine the was used to measure the adherence rate of PMN to VEC, while flow cytometry was used to determine the expression of CD54 and CD62E on the VEC surface. expression of CD54 and CD62E on the VEC surface. RESULTS: After 6 h of incubation with TNF-alpha, the adherence After 6 h of incubation with TNF-alpha, the adherence of PMN to HUVECs as well as the percentage of fluorescence-positive cells and mean fluorescence intensity of PMN to HUVECs as well as the percentage of fluorescence-positive cells and mean fluorescence intensity (MFI) of surface CD54 and CD62E in HUVECs increased significantly ( (MFI) of surface CD54 and CD62E in HUVECs increased significantly (P<0.01). Pre-treatment of HUVECs with <0.01). Pre-treatment of HUVECs with PrG (0.1-5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-alpha (PrG (0.1-5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-alpha (P<0.05). PrG <0.05). PrG (1-5 mmol/L) inhibited the VEC surface expression of CD62E and CD54 in a dose-dependent way ( (1-5 mmol/L) inhibited the VEC surface expression of CD62E and CD54 in a dose-dependent way (P<0.05). PrG <0.05). PrG at lower concentrations (0.001-0.1 mmol/L) showed no effect on CD54 expression, while it showed a slightly at lower concentrations (0.001-0.1 mmol/L) showed no effect on CD54 expression, while it showed a slightly increasing trend in CD62E expression (increasing trend in CD62E expression (P>0.05). ASA at 10 mmol/L had no obvious effect on the positive rate of >0.05). ASA at 10 mmol/L had no obvious effect on the positive rate of CD62E and CD54. CD62E and CD54. CONCLUSIONS: High concentrations of PrG (0.1-5 mmol/L) exert its inhibitory effect on cellular High concentrations of PrG (0.1-5 mmol/L) exert its inhibitory effect on cellular adherence of PMN to HUVECs, and its mechanism may be related to inhibiting surface expression of CD54 and adherence of PMN to HUVECs, and its mechanism may be related to inhibiting surface expression of CD54 and CD62E in HUVECs. Its action concentration was lower than that of ASA. CD62E in HUVECs. Its action concentration was lower than that of ASA.
Authors: Eleftherios S Xenos; Scott L Stevens; Michael B Freeman; David C Cassada; Mitchell H Goldman Journal: Ann Vasc Surg Date: 2005-05 Impact factor: 1.466
Authors: F Crea; L M Biasucci; A Buffon; G Liuzzo; C Monaco; G Caligiuri; A Kol; G Sperti; D Cianflone; A Maseri Journal: Am J Cardiol Date: 1997-09-04 Impact factor: 2.778
Authors: S Kapiotis; G Sengoelge; W R Sperr; M Baghestanian; P Quehenberger; D Bevec; S R Li; E J Menzel; A Mühl; D Zapolska; I Virgolini; P Valent; W Speiser Journal: Life Sci Date: 1996 Impact factor: 5.037