Received 26 February 2009; received in revised form 17 March 2009; accepted 26 March 2009.
Abstract
Colostrum, a nutrient-rich fluid produced by female mammals immediately after giving birth, is loaded with several immune, growth, and tissue repair factors. However, it remains unknown whether bovine colostrum has anti-inflammatory effects on intestinal epithelial cells (IEC). In this study, we aimed to investigate the anti-inflammatory effects of colostrum on IEC and to elucidate its molecular mechanisms. Human colon cancer HT-29 cells were stimulated with interleukin (IL)–1β with or without bovine colostrum. The effects of colostrum on nuclear factor κB (NF-κB) signaling in HT-29 cells were examined using real-time reverse transcriptase–polymerase chain reaction detect IL-8 and intracellar adhesion molecule-1 mRNA expression using a NF-κB-dependent reporter gene assay and an electrophoretic mobility shift assay. Furthermore, we assessed the expression levels of inhibitor protein of NF-κB–α, cyclooxygenase-2, and p65 proteins by Western blotting. Bovine colostrum significantly inhibited IL-1β-induced IL-8 and intracellar adhesion molecule-1 mRNA expression. Moreover, it suppressed IL-1β-induced NF-κB activation, including NF-κB dependent reporter gene expression in a dose-dependent manner. Finally, Western blotting revealed that colostrum decreased the cyclooxygenase-2 protein expression level, inhibited inhibitor protein of NF-κB–α degradation, and blocked translocation of p65 into the nucleus. These data demonstrated that bovine colostrum might protect against IEC inflammation by inhibiting the NF-κB pathway, suggesting colostrum has a therapeutic potential for intestinal inflammation.
Department of Internal Medicine and Institute of Gastroenterology, Brain Korea 21 Project for Medical Science, Yonsei University College of Medicine, Seoul, Korea
Corresponding author. Department of Internal Medicine, Yonsei University College of Medicine, 134 Shinchon-dong, Seodaemun-gu, 120-752 Seoul, Korea. Tel.: +82 2 2228 1990; fax: +82 2 393 6884.
☆ This study was supported by a grant from the Korea Healthcare Technology R&D Project, Ministry for Health, Welfare & Family Affairs, Republic of Korea (A084943).