ArticleMedical science monitor : international medical journal of experimental and clinical research2020
GTS-21 Promotes α7 nAChR to Alleviate Intestinal Ischemia-Reperfusion-Induced Apoptosis and Inflammation of Enterocytes.
Article in Medical science monitor : international medical journal of experimental and clinical research, 2020. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 5 papers.
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Who cites it
5 citing papers in PubMed, 8 citations in OpenAlex.
- Involvement of α7nAChR in the hepatic-protective effect of remifentanil preconditioning in ischemia/reperfusion rats.Hereditas · 2025Article
- Insights Into the Differential Desensitization ofMolecular pharmacology · 2023Article
- Tofacitinib protects intestinal epithelial cells against oxygen-glucose deprivation/reoxygenation injury by inhibiting the JAK/STAT3 signaling pathway.Experimental and therapeutic medicine · 2021Article
- Therapeutic Targeting ofPharmacological reviews · 2021Review
- Autonomic balance determines the severity of COVID-19 courses.Bioelectronic medicine · 2020Article
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Authors and funding
4 authors at 3 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
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 alpha7 nAChR has been shown to exert anti-inflammatory effects and anti-oxidation effects in various organs. However, whether alpha7 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 alpha7 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-alpha, IL-1ß, 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-alpha, IL-1ß, 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 alpha7 nAChR decreased the OGD/R-induced inflammatory response, oxidative damage, and apoptosis of intestinal epithelial cells.
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