RESUMO
<p><b>OBJECTIVE</b>To evaluate the effect of actovegin (Nycomed, deproteinized hemoderivative of calf blood injection) on intestinal mucosa in rats with acute radiation enteritis, and observe the changes of expression of apoptosis-related bcl-2/bax genes.</p><p><b>METHODS</b>An abdominal irradiation in a dose of 9.0 Gy X-ray of linear accelerator was performed once on a group of Wistar rats to establish a model of acute intestinal radiation enteritis. The experimental rats were randomly divided into five groups. Group 1 was normal control group; group 2 was model control group; groups 3, 4 and 5 were treated with low, middle and high dose of actovegin, respectively. After the model was established, actovegin injection was given intraperitoneally for successive 4 days. Corresponding intestinal tissues were taken for morphological examination with an image analysis system. The expression of apoptosis related bax and bcl-2 protein in the intestinal mucosal epithelial cells was determined by immunohistochemistry.</p><p><b>RESULTS</b>The groups 4 and 5 had significantly higher height of intestinal villi, the depth of crypt, the thickness of the mucosa and entire wall (254.66/261.71 microm, 166.47/165.41 microm, 510.44/511.71 microm, 610.38/608.98 microm), compared with those of the model control group (239.12 microm, 151.45 microm, 420.27 microm and 579.32 microm), respectively (P < 0.05). Treatment with middle and high doses of actovegin also significantly down-regulated the expression of activating apoptosis protein bax (24.54/23.24) compared with that of model control group (59.32) (P < 0.05) and up-regulated the expression of inhibiting apoptosis protein bcl-2 (55.54/52.21) compared with that of model control group (20.32) (P < 0.05). The ratio of bcl-2/bax was significantly higher in the groups 4 and 5 (2.2632, 2.1275) compared with that in the model control group (0.3425) (P < 0.01).</p><p><b>CONCLUSION</b>Actovegin accelerates the recovery of the acute radiation-injured intestinal mucosal epithelium by decreasing apoptosis via down-regulation of the expression of activating apoptosis protein bax and up-regulation of inhibiting apoptosis protein bcl-2.</p>