Effects of pentoxifylline and protein kinase C inhibitor on phorbol ester-induced intercellular adhesion molecule-1 expression in brain microvascular endothelial cells.
Abstract
AIM:
To study the potential roles of protein kinase C (PKC) on expression of intercellular adhesion molecule-1 (ICAM-1) in rat brain microvascular endothelial cells (RBMEC).
METHODS:
ICAM-1 expression in RBMEC was measured by ELISA analyses.
RESULTS:
Phorbol ester (PMA) enhanced the expression of ICAM-1 in a concentration (10-100 nmol.L-1) and time (4-16 h)-dependent manner in RBMEC. Pentoxifylline (PTX) 1-100 mumol.L-1 and the PKC inhibitor H7 5-50 mumol.L-1 prevented PMA-induced stimulation of ICAM-1 expression. At PTX 100 mumol.L-1 and H7 50 mumol.L-1, they reached maximal inhibitory effects [ICAM-1 expression (A) from (0.410 +/- 0.014) to (0.175 +/- 0.022) and (0.182 +/- 0.013), respectively; P < 0.01].
CONCLUSION:
Activation of PKC in RBMEC is associated with increased expression of ICAM-1 in RBMEC. PTX and H7 preincubation may inhibit PKC-induced up-regulation of ICAM-1.
Keywords:
To study the potential roles of protein kinase C (PKC) on expression of intercellular adhesion molecule-1 (ICAM-1) in rat brain microvascular endothelial cells (RBMEC).
METHODS:
ICAM-1 expression in RBMEC was measured by ELISA analyses.
RESULTS:
Phorbol ester (PMA) enhanced the expression of ICAM-1 in a concentration (10-100 nmol.L-1) and time (4-16 h)-dependent manner in RBMEC. Pentoxifylline (PTX) 1-100 mumol.L-1 and the PKC inhibitor H7 5-50 mumol.L-1 prevented PMA-induced stimulation of ICAM-1 expression. At PTX 100 mumol.L-1 and H7 50 mumol.L-1, they reached maximal inhibitory effects [ICAM-1 expression (A) from (0.410 +/- 0.014) to (0.175 +/- 0.022) and (0.182 +/- 0.013), respectively; P < 0.01].
CONCLUSION:
Activation of PKC in RBMEC is associated with increased expression of ICAM-1 in RBMEC. PTX and H7 preincubation may inhibit PKC-induced up-regulation of ICAM-1.