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Effects of Propyl Gallate on adhesion of polymorphonuclear leukocytes to human endothelial cells induced by tumor necrosis factor alpha
Effects of Propyl Gallate on adhesion of polymorphonuclear leukocytes to human endothelial cells induced by tumor necrosis factor alpha
- 中国结合医学杂志（英文版） 2009年15卷第1期 页码：47-53
- Affiliations：
1. Department of Cardiovascular Diseases, Xiyuan Hospital, China Academy of Chinese Medical Sciences,Beijing,China
2. Laboratory of Hematopathy, Xiyuan Hospital, China Academy of Chinese Medical Sciences,Beijing,China
- Author bio：
- Funds：Supported by the National Natural Science Foundation of China (No. 90409021)
DOI：10.1007/s11655-009-0047-3
中图分类号：纸质出版日期：2009，
网络出版日期：2009-3-7，
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Jiang, Yr., Chen, Kj., Xu, Yg. et al. Effects of Propyl Gallate on adhesion of polymorphonuclear leukocytes to human endothelial cells induced by tumor necrosis factor alpha., Chin. J. Integr. Med. 15, 47–53 (2009). https://doi.org/10.1007/s11655-009-0047-3
Yue-rong Jiang, Ke-ji Chen, Yong-gang Xu, et al. Effects of Propyl Gallate on adhesion of polymorphonuclear leukocytes to human endothelial cells induced by tumor necrosis factor alpha[J]. Chinese Journal of Integrative Medicine, 2009,15(1):47-53.
Jiang, Yr., Chen, Kj., Xu, Yg. et al. Effects of Propyl Gallate on adhesion of polymorphonuclear leukocytes to human endothelial cells induced by tumor necrosis factor alpha., Chin. J. Integr. Med. 15, 47–53 (2009). https://doi.org/10.1007/s11655-009-0047-3 DOI：
Yue-rong Jiang, Ke-ji Chen, Yong-gang Xu, et al. Effects of Propyl Gallate on adhesion of polymorphonuclear leukocytes to human endothelial cells induced by tumor necrosis factor alpha[J]. Chinese Journal of Integrative Medicine, 2009,15(1):47-53. DOI： 10.1007/s11655-009-0047-3.
摘要
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. A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-α). VECs were pre- A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-α). VECs were preincubated with varying concentrations of PrG (0.001–5 mmol/L) or 1‰ DMSO (v:v) or 10 mmol/L acetylsalicylic incubated with varying concentrations of PrG (0.001–5 mmol/L) or 1‰ DMSO (v:v) or 10 mmol/L acetylsalicylic acid (ASA) for 1 h
and then were stimulated with 10 ng/mL TNF-α for 6 h. Rose bengal vital staining method acid (ASA) for 1 h
and then were stimulated with 10 ng/mL TNF-α 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. After 6 h of incubation with TNF-α
the adherence After 6 h of incubation with TNF-α
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-α (PrG (0.1–5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-α (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. 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.
Abstract
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. A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-α). VECs were pre- A human VEC inflammation model was induced by tumor necrosis factor alpha (TNF-α). VECs were preincubated with varying concentrations of PrG (0.001–5 mmol/L) or 1‰ DMSO (v:v) or 10 mmol/L acetylsalicylic incubated with varying concentrations of PrG (0.001–5 mmol/L) or 1‰ DMSO (v:v) or 10 mmol/L acetylsalicylic acid (ASA) for 1 h
and then were stimulated with 10 ng/mL TNF-α for 6 h. Rose bengal vital staining method acid (ASA) for 1 h
and then were stimulated with 10 ng/mL TNF-α 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. After 6 h of incubation with TNF-α
the adherence After 6 h of incubation with TNF-α
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-α (PrG (0.1–5 mmol/L) significantly suppressed the adherence of PMN to VECs induced by TNF-α (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. 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.
关键词
cellular adhesionintercellular adhesion molecule-1E-selectinpropyl gallate
Keywords
cellular adhesionintercellular adhesion molecule-1E-selectinpropyl gallate
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