The Study On The Identification Of Types Of Enterocyte Death And The Expression Of Modificative P53Protein In The Mice Model Of Intestinal Radiation Sickness

Objective Radiotherapy is one of the three major methods in tumor therapy,70percent of malignancies need radiotherapy. The patients have intestinal symptomsduring radiotherapy in many intraabdominal malignancies, for example, diarrhea,dyspepsia et al. This is the side effect caused by the damage of intestinal normal cellswith radiotherapy. This side effect influences the process of radiotherapy and therecovery of patients immensely. Furthermore, there is no effective drug to treat theintestinal radiation sickness in the accident of nuclear leakage. According to theresearch of the types of enterocyte death and its mechanism after irradiation, hope toenhance the protection of normal tissues, increase the effect of radiotherapy and treatthe intestinal radiation sickness.Methods The ilea from mice with15Gy whole body irradiation (WBI) weredrawn, morphological features observed by hematoxylin&eosin (HE) staining andTransmission electron micrographs (TEM); the lever of reactive oxygen species(ROS)was analyzed by immunofluorescence; the lever of glutathione(GSH), nitric oxide(NO),hydrogen peroxide(H2O2) and superoxide dismutase(SOD) were analyzed by ELISA;the biochemical features were analyzed by Western blotting of caspase3&Light Chain3(LC3) B, Immunofluorescence of High mobility group box chromosomal protein(HMGB)1, Enzyme Linked Immunosorbent Assay (ELISA) of interleukin (IL)6in theserum.Results The lever of reactive oxygen species(ROS) in the ilea increasedobviously after irradiation, but the oxidation index（GSH, NO, H2O2, SOD）do notchange obviously; the apoptotic, necrotic, and autophagic features of mice ilea after15Gy whole body irradiation (WBI) are shown. The data were obtained usingmorphological and the biochemical features: the presence of cleaved caspase (apoptosismarker), conversion from Light Chain3(LC3)-I to (LC3)-II (autophagy marker), secretion of serum interleukin (IL)-6, and the expression and secretion of highmobility group box chromosomal protein (HMGB)1(necrosis marker). Tp53acetylation at lysine379and Tp53phosphorylation at Ser6/20/392was induced afterirradiation, which disappeared at2h after WBI.Conclusion The death of enterocytes could not be classified into one type of celldeath but rather as “mixed death.” Therapeutic agents that promote Tp53acetylation atlysine379and Tp53phosphorylation at Ser6/20/392could decrease the enterocytedeath and prolong survival after radiation therapy.