Abstract
Notch signaling is associated with the pathogenesis of ulcerative colitis (UC). This study investigated whether the Notch regulates intestinal epithelial cell apoptosis and reactive oxygen species (ROS) production. Rats were separated into UC model group and control group followed by analysis of the expression of Notch1, Hes1 and OLFM4 by real-time PCR and western blot, content of malondialdehyde (MDA), superoxide dismutase (SOD) and caspase-3 as well as cell apoptosis by flow cytometry. Under LPS stimulation conditions, IEC-6 cells were divided into LPS + siRNA-NC group and LPS + siRNA-Notch1 group and Notch1, Hes1 and OLFM4 level as well as ROS was measured. Compared with control group, the activity of caspase-3, MDA and apoptosis in colon tissue of UC model were significantly increased with decreased SOD activity and increased Notch1, Hes1 and OLFM4 expression. LPS treatment can significantly up-regulate the expression of Notch1, Hes1 and OLFM4 in IEC-6 cells, increase cell apoptosis and ROS production. Notch1 interference by siRNA significantly downregulated Notch1, Hes1, and OLFM4 in IEC cells, and increased cell apoptosis and ROS production. UC lesions can activate Notch signaling pathway in colon tissue, which may play a role in repair. Interference with Notch1 signaling may aggravate intestinal epithelial cell apoptosis and ROS production in an inflammatory environment.
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