The mechanisms of thalidomide in treatment of angiodysplasia due to hypoxia
10.3760/cma.j.issn.0578-1426.2009.04.011
- VernacularTitle:沙立度胺抑制缺氧所致胃肠道血管发育不良的机制初探
- Author:
Huimin CHEN
;
Zhizheng GE
;
Wenzhong LIU
;
Hong LU
;
Chunhong XU
;
Jingyuan FANG
;
Shudong XIAO
- Publication Type:Journal Article
- Keywords:
Thalidomide;
Anoxia;
Angiodysplasia;
Vascular endothelial growth factors;
HIF-α
- From:
Chinese Journal of Internal Medicine
2009;48(4):295-298
- CountryChina
- Language:Chinese
-
Abstract:
Objective To investigate the inhibitory effect of thalidomide on angiodysplasia.Methods Excisional intestinal specimens were collected and immunohistochemical examination was carried out.The human umbilical vein endothelial cells were cultured in vitro to exponential phase of growth,divided into six groups and synchronized for 24 hours.They were then stimulated with thalidomide (40-100 μg/ml) for 72 hours.MTT assay was used to assess cellular proliferation.ELISA,real-time quantitative PCB and western blot were applied to detect the expression of VEGF/HIF-1α of human umbilical vein endothelial cells (HUVEC).Results Immunohistochemical analysis of intestinal pathological specimens demonstrated higher expression of VEGF.ELISA showed that the expression of VEGF under hypoxia was obviously higher than that under normoxia [ ( 1199.3 ± 61.4) ng/L vs ( 864.7 ± 41.2 ) ng/L,P < 0.05 ].Real-time quantitative PCR and Western blot discovered that thalidomide inhibited the expression of VEGF/ HIF-1α of HUVEC (P < 0.05).The effect of thalidomide was dose-dependent.Conclusions Thalidomide can suppress the expression of HIF-1α and VEGF in HUVEC in vitro and then inhibit angiodysplasia,which may play a significant role in stopping the rebleeding in patients with recurrent gastrointestinal bleeding.
