염증성 창자질환에서의 유전자 손상복구 반응

Abstract

Oxidative stress is an imbalance condition between production of reactive oxygen species (ROS) and diminished antioxidant defense systems. Oxidative stress develops chiefly in the processing ofinflammations since the inflammatory cells create enormous volume of ROS for the purpose of protection from many noxious assaults. It has been extensively identified extensively that oxidative stress in inflammatory tissue can head for malignant growth. Moreover oxidative stress acts as a chief pathogenetic factor for cancer development from inflammatory diseases, such as chronic inflammatory bowel disease (IBD)-related colorectal cancer. The levels of oxidized bases in the DNA molecule are a result of the balance between the amount of oxidative DNA damage and repair. Thereforewe analyzed the changes of colonic mucosal DNA repair proteins of the dextran sulfate sodium(DSS)-induced IBD. In this experiment, we studied the DSS- induced colonic mucosal changesof morphological localization and protein expression for DNA base mismatch repair(MMR) proteins, MSH2, MSH6; DNA base damage marker and base excision repair(BER) protein, 8-oxo-7,8-dihydro-2,-deoxyguanosine (8OHdG), Ref1, OGG1; DNA double strands breaks(DSB) marker and its repair(BER) protein, -H2AX, DNAPKCs, Ku70, Ku80. The patterns of DNA repair proteins expression were protein-specific with time-course. While the DNA repair proteins that show increased expression were Ref-1, OGG1, DNAPKCs and MSH2, but Ku80 was decreased. The proteins changed level of expression may be the target molecule in the pathogenesis and protection of IBD, but additional study are needed to be confirmed.