Celecoxib, a selective cyclooxygenase-2 inhibitor, aggravates radiation-induced intestinal damage in mice

서지정보

ㆍ발행기관 : 충북대학교 동물의학연구소 ㆍ수록지정보 : Journal of Biomedical and Translational Research / 22권 / 1호
ㆍ저자명 : Sueun Lee, Jin Mi Chun, Ji Hye Lee, Yun-Soo Seo, Jun Hong Park, Hae-June Lee, Changjong Moon, Sung-Ho Kim, Joong-Sun Kim

목차

Introduction
Materials and Methods
Animal maintenance and study schedule
Immunohistochemistry
Western blotting
Quantitative reverse transcription-polymerase chainreaction (qRT-PCR) analysis
Statistical analysis
Results
Effect of celecoxib on intestinal morphological changesin irradiated mice
Effect of celecoxib on COX-2 expression in theintestine of irradiated mice
Discussion
References

영어 초록

Celecoxib, a cyclooxygenase (COX)-2 selective inhibitor, was approved as a non-steroidal anti-inflammatory drug (NSAID), and this therapeutic application has been expanded to several other diseases, including colon cancer. Notably, a treatment strategy combining the use of celecoxib and radiation therapy has been employed for improving the control of local cancers. In this study, we examined the effect of celecoxib on irradiation-induced intestinal damage. The twenty four mice (BALB/c) were divided into four groups; 1) sham-irradiated control group, 2) celecoxib-treated group, 3) irradiated group, and 4) celecoxib-treated irradiation group. Mice were orally administered celecoxib at a dose of 25 mg/kg in a 0.1 mL volume, daily for 4 days after irradiation exposure (10 Gy). Then, histological examinations of the jejunal villous height, crypt survival, and crypt size were performed. The expression of COX-2 after administration of celecoxib in irradiated mice was examined by employing immunohistochemistry, Western blotting, and qPCR analysis. The jejunal villi height and the crypt survival were reduced in the irradiation group compared with the sham-irradiated group. Celecoxib treatment in irradiation mice even more decreased those indicators. Crypt size was increased in the radiation group compared to the sham-irradiated control group, whereas the size was decreased in the celecoxibtreated irradiation group compared with the group exposed to the radiation injury. COX-2 expression was detected in the crypt of the small intestine, and COX-2 expression was increased in the crypt lesion following radiation exposure. However, COX-2 expression was reduced in the celecoxib-treated irradiation group. Therefore, in the present study, we confirmed that celecoxib treatment after irradiation aggravated the irradiation-induced intestinal damage. These results suggest that a caution need to be administered when celecoxib treatment is performed in combination with radiation therapy for cancer treatment.

참고 자료

없음