Thalidomide effect in endothelial cell of acute radiation proctitis.
OBJECTIVE
To determine whether thalidomide prevents microvascular injury in acute radiation proctitis in white rats.


METHODS
Fourteen female Wistar rats were used: six in the radiation group, six in the thalidomide group, and two in normal controls. The radiation and thalidomide groups were irradiated at the pelvic area using a single 30 Gy exposure. The thalidomide (150 mg/kg) was injected into the peritoneum for 7 d from the day of irradiation. All animals were sacrificed and the rectums were removed on day 8 after irradiation. The microvessels of resected specimens were immunohistochemically stained with thrombomodulin (TM), von Willebrand Factor (vWF), and vascular endothelial growth factor (VEGF).


RESULTS
The microscopic scores did not differ significantly between the radiation and thalidomide groups, but both were higher than in the control group. Expression of TM was significantly lower in the endothelial cells (EC) of the radiation group than in the control and thalidomide groups (P<0.001). The number of capillaries expressing vWF in the EC was higher in the radiation group (15.3+/-6.8) than in the control group (3.7+/-1.7), and the number of capillaries expressing vWF was attenuated by thalidomide (10.8+/-3.5, P<0.001). The intensity of VEGF expression in capillaries was greater in the radiation group than in the control group and was also attenuated by thalidomide (P=0.003).


CONCLUSIONS
The mechanisms of acute radiation-induced proctitis in the rats are related to endothelial cell injury of microvessel, which may be attenuated with thalidomide.
Kim
Ki-Tae
KT
Department of Internal Medicine, College of Medicine, The Catholic University of Korea, Uijeongbu St. Mary's Hospital, 65-1 Geumo-dong, Uijeongbu city, Kyunggido 480-717, South Korea. chs@catholic.ac.kr
Chae
Hiun-Suk
HS
Kim
Jin-Soo
JS
Kim
Hyung-Keun
HK
Cho
Young-Seok
YS
Choi
Whang
W
Choi
Kyu-Yong
KY
Rho
Sang-Young
SY
Kang
Suk-Jin
SJ
D000818:Animals; D042783:Endothelial Cells / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D005260:Female; D008833:Microcirculation / Q000187:drug effects; D011349:Proctitis / Q000473:pathology / Q000517:prevention & control*; D011833:Radiation Injuries, Experimental / Q000473:pathology / Q000517:prevention & control*; D011837:Radiation-Protective Agents / Q000494:pharmacology*; D051381:Rats; D017208:Rats, Wistar; D012007:Rectum / Q000187:drug effects* / Q000378:metabolism / Q000473:pathology / Q000528:radiation effects; D013792:Thalidomide / Q000494:pharmacology*; D018180:Thrombomodulin / Q000378:metabolism; D042461:Vascular Endothelial Growth Factor A / Q000378:metabolism; D014841:von Willebrand Factor / Q000378:metabolism
D011837:Radiation-Protective Agents; D018180:Thrombomodulin; D042461:Vascular Endothelial Growth Factor A; C467498:vascular endothelial growth factor A, rat; D014841:von Willebrand Factor; D013792:Thalidomide