TY - JOUR
T1 - Anti-angiogenic effects of Shiraiachrome A, a compound isolated from a Chinese folk medicine used to treat rheumatoid arthritis
AU - Tong, Yunguang
AU - Zhang, Xiongwen
AU - Zhao, Weimin
AU - Zhang, Yixiang
AU - Lang, Jingyu
AU - Shi, Yuhua
AU - Tan, Wenfu
AU - Li, Meihong
AU - Zhang, Yongwei
AU - Tong, Linjiang
AU - Lu, He
AU - Lin, Liping
AU - Ding, Jian
PY - 2004/6/28
Y1 - 2004/6/28
N2 - The Chinese folk medicine Shiraia bambusicola has long been utilized in the treatment of rheumatoid arthritis, a disease in which angiogenesis plays an important role. We report here the isolation of the compound Shiraiachrome A from S. bambusicola and the demonstration of its anti-angiogenic properties. We found that Shiraiachrome A significantly inhibited the proliferation, migration, and tube formation of human microvascular endothelial cells (HMEC) in a dose-dependent manner, with average IC50 values of 2.1±0.36, 1.97±0.44, and 1.65±0.59 μM, respectively. In addition, Shiraiachrome A inhibited the formation of new microvessels in a rat aorta culture model as well as in the chick embryo chorioallantoic membrane (CAM) assay. Investigation of the mechanism of action of Shiraiachrome A demonstrated that this compound suppressed the autophosphorylation of four receptor tyrosine kinases (RTKs), with IC50 values ranging from 2.2 to 4.3 μM. These results suggest that Shiraiachrome A inhibits angiogenesis by blocking growth factor-stimulated autophosphorylation of RTKs. These findings also indicate that Shiraiachrome A may be a potent therapeutic agent for angiogenesis-related diseases such as cancer, rheumatoid arthritis, and diabetic retinopathy.
AB - The Chinese folk medicine Shiraia bambusicola has long been utilized in the treatment of rheumatoid arthritis, a disease in which angiogenesis plays an important role. We report here the isolation of the compound Shiraiachrome A from S. bambusicola and the demonstration of its anti-angiogenic properties. We found that Shiraiachrome A significantly inhibited the proliferation, migration, and tube formation of human microvascular endothelial cells (HMEC) in a dose-dependent manner, with average IC50 values of 2.1±0.36, 1.97±0.44, and 1.65±0.59 μM, respectively. In addition, Shiraiachrome A inhibited the formation of new microvessels in a rat aorta culture model as well as in the chick embryo chorioallantoic membrane (CAM) assay. Investigation of the mechanism of action of Shiraiachrome A demonstrated that this compound suppressed the autophosphorylation of four receptor tyrosine kinases (RTKs), with IC50 values ranging from 2.2 to 4.3 μM. These results suggest that Shiraiachrome A inhibits angiogenesis by blocking growth factor-stimulated autophosphorylation of RTKs. These findings also indicate that Shiraiachrome A may be a potent therapeutic agent for angiogenesis-related diseases such as cancer, rheumatoid arthritis, and diabetic retinopathy.
KW - Angiogenesis inhibitor
KW - Arthritis
KW - Receptor tyrosine kinase
KW - Shiraiachrome A
UR - https://www.scopus.com/pages/publications/2942701976
U2 - 10.1016/j.ejphar.2004.04.053
DO - 10.1016/j.ejphar.2004.04.053
M3 - 文章
C2 - 15212963
AN - SCOPUS:2942701976
SN - 0014-2999
VL - 494
SP - 101
EP - 109
JO - European Journal of Pharmacology
JF - European Journal of Pharmacology
IS - 2-3
ER -
