Open AccessThe protective effects of XH‐105 against radiation‐induced intestinal injury
Author(s) -
Cheng Ying,
Dong Yinping,
Hou Qinlian,
Wu Jing,
Zhang Wei,
Tian Hongqi,
Li Deguan
Publication year - 2019
Publication title -
journal of cellular and molecular medicine
Language(s) - English
Resource type - Journals
SCImago Journal Rank - 1.44
H-Index - 130
eISSN - 1582-4934
pISSN - 1582-1838
DOI - 10.1111/jcmm.14159
Subject(s) - apoptosis , crypt , dna damage , lgr5 , small intestine , radiation enteritis , radiation injury , acute radiation syndrome , jejunum , chemistry , cancer research , biology , medicine , enteritis , stem cell , radiation therapy , gastroenterology , microbiology and biotechnology , biochemistry , dna , cancer stem cell , haematopoiesis
Radiation‐induced intestinal injury is one of the major side effects in patients receiving radiation therapy. There is no specific treatment for radiation enteritis in the clinic. We designed and synthesized a new compound named XH‐105, which is expected to cleave into polyphenol and aminothiol in vivo to mitigate radiation injury. In the following study, we describe the beneficial effects of XH‐105 against radiation‐induced intestinal injury. C57BL/6J mice were treated by gavage with XH‐105 1 hour before total body irradiation (TBI), and the survival rate was monitored. Histological changes were examined, and survival of Lgr5 + intestinal stem cells Ki67 + cells, villi + enterocytes and lysozymes was determined by immunohistochemistry. DNA damage and cellular apoptosis in intestinal tissue were also evaluated. Compared to vehicle‐treated mice after TBI, XH‐105 treatment significantly enhanced the survival rate, attenuated structural damage of the small intestine, decreased the apoptotic rate, reduced DNA damage, maintained cell regeneration and promoted crypt proliferation and differentiation. XH‐105 also reduced the expression of Bax and p53 in the small intestine. These data suggest that XH‐105 is beneficial for the protection of radiation‐induced intestinal injury by inhibiting the p53‐dependent apoptosis signalling pathway.