Abstract
Objective To obesrve the effects of carbon monoxide release molecule-2 (CORM-2) on intestinal barrier injury in breast cancer rats. Methods Sixty female Sprague-Dawley rats were selected as the study subjects, and were randomly divided into sham operation group, breast tumor group, CORM-2 group and iCORM-2 group (inactivated CORM-2), 15 each. Both the CORM-2 group and the iCORM-2 group were intraperitoneally injected with 5 mg/kg of the interventional drug 1 h before the preparation of the breast tumor model. The model was used or the ileum was collected 24 hours after operation. The expression of Occludin, ZO-1 and Claudin3 protein in the ileum was detected by Western blotting. Blood D-lactic acid, tumor necrosis factor-α (TNF-α) and intestinal type were detected by enzyme linked immunosorbent assay (ELISA). The levels of fatty acid binding protein (I-FABP), diamine oxidase (DAO) and myeloperoxidase (MPO) were detected by polymerase chain reaction (RT-PCR). Rho kinase-1 mRNA and ROCK-2 mRNA were detected in small intestinal mucosa. The effect of CORM-2 on intestinal barrier injury in breast cancer rats was analyzed. Results The expressions of Occludin (0.07±0.01, 0.13±0.02), ZO-1 (0.09±0.03, 0.12±0.02) and Claudin3 (0.21±0.03, 0.24±0.06) in the breast tumor group and iCORM-2 group were lower than those in the iCORM-2 group. Sham operation group (0.35±0.04, 0.49±0.05, 0.64±0.07) and CORM-2 group (0.33±0.03, 0.23±0.04, 0.42±0.05), low expression levels of ZO-1 and Claudin3 in CORM-2 group In the sham operation group, the difference was statistically significant (t=2.389, 2.186, 2.801, P 0.05). Rho kinase-1 mRNA (1.03±0.04, 3.27±0.07, 2.21±0.05) and ROCK-2 mRNA (0.78±0.08, 2.24±0.12, 2.17±0.17) in small intestinal mucosa of breast tumor group, CORM-2 and iCORM-2 group. The Rho kinase-1 mRNA in the small intestinal mucosa of the CORM-2 group was lower than that of the breast tumor group and the iCORM-2 group (F=7.831, 8.427, 4.997, P 0.05). Conclusion CORM-2 can alleviate intestinal barrier damage, inhibit the release of inflammatory mediators, enhance the tight relationship between intestinal epithelial cells, increase intestinal mucosal permeability and protect intestinal barrier. Key words: Breast neoplasms; Rats; Carbon monoxide release molecule-2; Intestinal barrier
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