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Apoptosis, necrosis, and autophagy in mouse intestinal damage after 15‐Gy whole body irradiation
Author(s) -
Chen Qiu,
Xia Xiaochun,
Wu Shu,
Wu Anqing,
Qi Dandan,
Liu Wei,
Cui Fengmei,
Jiao Yang,
Zhu Wei,
Gu Yongping,
Gao Hongjian,
Zhang Xueguang,
Cao Jianping
Publication year - 2014
Publication title -
cell biochemistry and function
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 0.933
H-Index - 61
eISSN - 1099-0844
pISSN - 0263-6484
DOI - 10.1002/cbf.3068
Subject(s) - necrosis , apoptosis , programmed cell death , autophagy , necroptosis , h&e stain , tumor necrosis factor alpha , caspase , ileum , biology , staining , microbiology and biotechnology , pathology , andrology , medicine , immunology , endocrinology , biochemistry
Enterocytes die during high‐dose radiation exposure in radiation accidents. The modality of cell death has a profound effect on the therapeutic response. The ilea from mice with 15 Gy total body irradiation (TBI) were drawn, morphological features observed by hematoxylin and eosin staining and transmission electron micrographs. The biochemical features of mouse ileum presented with the structure were cleaved Caspase‐3 (apoptosis marker), Light Chain 3 (LC3)‐I's conversion to LC3‐II (autophagy marker) and high mobility group box chromosomal protein 1's secretion (necrosis marker). Then, the autophagy inhibitor (3‐methyladenine), caspase inhibitor (Z‐VAD‐FMK) or necrosis inhibitor (necrostatin) was used to prevent death. Apoptosis, autophagy and necrosis were all appeared in the ileum, but necrosis had the biggest size; the use of 3‐methyladenine and Z‐VAD‐FMK prolong one day's life of the mice after 15 Gy TBI, necrostatin significantly extended the lifespan of 15 Gy irradiated mice ( p < 0.05). The results suggest that the death of enterocytes could not be classified into one type of cell death but rather as ‘mixed death.’ Copyright © 2014 John Wiley & Sons, Ltd.