BACKGROUND: Intestinal ischemia-reperfusion injury is a serious intestinal disease, with main symptoms of inflammatory reaction and severe oxidative damage. In addition, GTS-21-induced α7 nAChR has been shown to exert anti-inflammatory effects and anti-oxidation effects in various organs. However, whether α7 nAChR can alleviate ischemia-reperfusion-induced intestinal injury is unclear.

MATERIAL AND METHODS: We used intestinal epithelial cells (IEC-6) to perform the experiments. Oxygen glucose deprivation/reoxygenation (OGD/R) was used to simulate the physiological environment of ischemia-reperfusion. First, the expression of α7 nAChR was determined in these cells which was cultured under OGD/R conditions. After that, the GTS-21 was used to treat these cells and the levels of inflammatory factors (TNF-α, IL-1β, IL-6, and IL-10) were assessed by ELISA. Next, the levels of ROS, SOD, and MDA were determined in IEC-6 cells. Finally, the apoptosis rates of IEC-6 cells were measured by flow cytometry.

RESULTS: Results showed that the expression of TNF-α, IL-1β, and IL-6 was enhanced when the IEC-6 cells were cultured under OGD/R conditions. However, after treatment with GTS-21, the levels of these proinflammatory factors were suppressed. In addition, the levels of ROS and MDA were also inhibited and the expression of SOD was promoted after GTS-21 treatment. We also found that the ratios of apoptotic cells declined after GTS-21 treatment.

CONCLUSIONS: GTS-21-induced α7 nAChR decreased the OGD/R-induced inflammatory response, oxidative damage, and apoptosis of intestinal epithelial cells.

Keywords: Intestinal Diseases, Benzylidene Compounds, Cytokines, Enterocytes, Glucose, Intestinal Mucosa, Intestines, NF-E2-Related Factor 2, Oxygen, Reperfusion, alpha7 Nicotinic Acetylcholine Receptor