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X irradiation induced colonic mucosal injury and the detection of apoptosis through PARP-1/p53 regulatory pathway

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dc.creator ÖZ, ZEHRA SAFİ
dc.creator Kececi, Mete
dc.creator GÜLLE, Kanat
dc.date 2020-06-30T21:00:00Z
dc.date.accessioned 2021-01-21T07:50:27Z
dc.date.available 2021-01-21T07:50:27Z
dc.identifier 023b0d9d-0e91-4a68-8db8-963ed794957e
dc.identifier 10.1016/j.biopha.2020.110134
dc.identifier https://avesis.sdu.edu.tr/publication/details/023b0d9d-0e91-4a68-8db8-963ed794957e/oai
dc.identifier.uri http://acikerisim.sdu.edu.tr/xmlui/handle/123456789/78044
dc.description This study aimed to explore whether PARP-1 regulatory pathway mediated X irradiation induced cell cycle arrest and apoptosis or not. In this regard, colonic mucosal injury caused by whole-body X-irradiation induced apoptosis through PARP-1, caspase 3 and p53 regulatory pathway were evaluated in experimental rat models. Eighteen Wistar albino rats were divided into three groups. Two radiation groups received 8.3 Gy dose of whole-body X-irradiation as a single dose and the control group received physiological saline intraperitoneally. Radiation groups were sacrificed after 6 h and 4 days of irradiation. PARP-1 and caspase 3 expression in the nuclei of colonic crypt cells significantly increased 6 h after irradiation, and declined 4 days after irradiation. In conflict with other studies that reported p53 as not being expressed widely in colonic mucosa, in our study the expressions of p53 were elevated both in the cytoplasm and in the nucleus of the crypt cells, especially 6 h after irradiation. In the radiation groups, colonic mucosal injury score was significantly elevated compared with that of the control group. Our data demonstrated that PARP-1, caspase-3 and p53 expression increased in colonic mucosa 6 h after irradiation.
dc.language eng
dc.rights info:eu-repo/semantics/closedAccess
dc.title X irradiation induced colonic mucosal injury and the detection of apoptosis through PARP-1/p53 regulatory pathway
dc.type info:eu-repo/semantics/article

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