TY - JOUR
T1 - Effects of monocrotaline pyrrole on morphology, number and production of nitric oxide of cultured artery endothelial cells
AU - Cheng, W.
AU - Li, Z.
AU - Koyama, T.
AU - Oike, M.
AU - Ito, Y.
N1 - Copyright:
Copyright 2004 Elsevier Science B.V., Amsterdam. All rights reserved.
PY - 2001
Y1 - 2001
N2 - Experimental model of pulmonary hypertension has been created by exposing animals to monocrotaline pyrrole (MCTP), but the cause of pulmonary hypertension induced by MCTP is still controversial. In this study, cell culture and DAF-2 fluorescence technique were used to investigate the effects of MCTP on Cell surface area, cell number and production of nitric oxide (NO) in cultured calf pulmonary artery endothelial cells (CPAE) and bovine aorta . endothelial cells (BAEC). MCTP induced the cell enlargement from (46 ± 4) to (223 ± 27) μm2 and decreased the number of cells from (175 ± 9) × 106 L-1 to (49 ± 6) × 106 L-1 in CPAE. Acetylcholine induced production of NO, measured by DAF-2, was decreased significantly from (16.1 ± 1.3) % to (1.5 ± 1.1)% and from (14.2 ± 1.6)% to (1.4 ± 1.6) % in CPAE and BAEC, respectively. The results indicate that MCTP may damage endothelial cells and inhibit NO production, which maybe another pathogenesis of MCTP induced pulmonary hypertension.
AB - Experimental model of pulmonary hypertension has been created by exposing animals to monocrotaline pyrrole (MCTP), but the cause of pulmonary hypertension induced by MCTP is still controversial. In this study, cell culture and DAF-2 fluorescence technique were used to investigate the effects of MCTP on Cell surface area, cell number and production of nitric oxide (NO) in cultured calf pulmonary artery endothelial cells (CPAE) and bovine aorta . endothelial cells (BAEC). MCTP induced the cell enlargement from (46 ± 4) to (223 ± 27) μm2 and decreased the number of cells from (175 ± 9) × 106 L-1 to (49 ± 6) × 106 L-1 in CPAE. Acetylcholine induced production of NO, measured by DAF-2, was decreased significantly from (16.1 ± 1.3) % to (1.5 ± 1.1)% and from (14.2 ± 1.6)% to (1.4 ± 1.6) % in CPAE and BAEC, respectively. The results indicate that MCTP may damage endothelial cells and inhibit NO production, which maybe another pathogenesis of MCTP induced pulmonary hypertension.
UR - http://www.scopus.com/inward/record.url?scp=0034951593&partnerID=8YFLogxK
UR - http://www.scopus.com/inward/citedby.url?scp=0034951593&partnerID=8YFLogxK
M3 - Article
AN - SCOPUS:0034951593
SN - 1000-3002
VL - 15
SP - 169
EP - 171
JO - Chinese Journal of Pharmacology and Toxicology
JF - Chinese Journal of Pharmacology and Toxicology
IS - 3
ER -