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Zhonghua nei ke za zhi [Chinese journal of internal medicine] 2009-Apr

[The mechanisms of thalidomide in treatment of angiodysplasia due to hypoxia].

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Hui-Min Chen
Zhi-Zheng Ge
Wen-Zhong Liu
Hong Lu
Chun-Hong Xu
Jing-Yuan Fang
Shu-Dong Xiao

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Abstrak

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 microg/ml) for 72 hours. MTT assay was used to assess cellular proliferation. ELISA, real-time quantitative PCR and western blot were applied to detect the expression of VEGF/HIF-1alpha 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-1alpha of HUVEC (P < 0.05). The effect of thalidomide was dose-dependent.

CONCLUSIONS

Thalidomide can suppress the expression of HIF-1alpha 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.

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