Immunoregulatory role of melatonin in Helicobacter pylori‐induced gastric diseases

Melatonin has shown important immunoregulatory activities in inflammatory disorders; however, the immunoregulatory role of melatonin in Helicobacter pylori‐induced gastric diseases remains unclear until now. This study aimed to examine the in‐vivo activity of melatonin against H. pylori‐induced gastric diseases and explore the immunoregulatory mechanisms. HE staining showed obvious inflammatory cell infiltration in the gastric mucosa and submucosa, and the culture of the mouse stomach homogenate was positive for the rapid urease test. Immunohistochemistry revealed extensive MT1 and MT2 expression in the gastric mucosa of H. pylori‐infected mice. ELISA measured lower TGF‐β1 levels in the liver of H. pylori‐infected mice than in uninfected mice 2 weeks post‐treatment with 25, 50 or 100 mg/kg melatonin, while higher TGF‐β1 levels were detected 4 and 6 weeks post‐treatment. Western blotting determined lower Foxp3 expression in the spleen of infected mice than in uninfected mice 2 weeks post‐treatment with 25, 50 or 100 mg/kg melatonin, and higher Foxp3 levels were detected 4 weeks post‐treatment with 50 and 100 mg/kg melatonin; however, the Foxp3 level was comparative in infected and uninfected mice 6 weeks post‐treatment. In addition, higher RORβ expression was found in the gastric specimens of infected mice than in uninfected mice 2 weeks post‐treatment with 25, 50 or 100 mg/kg melatonin, and higher RORβ expression was detected 6 weeks post‐treatment with 25 mg/kg melatonin. At 2, 4 and 6 weeks post‐treatment with 25, 50 and 100 mg/kg melatonin, higher TGF‐β1 expression was detected in the liver of infected mice than in uninfected mice. The results demonstrate that melatonin may alleviate H. pylori‐induced gastric diseases through mediating TGF‐β1 and Foxp3 expression via membrane and nuclear receptors.Support or Funding InformationNational Natural Science Foundation Youth Fund:81302601 NSFC(National Natural Science Foundation of China):30971541This abstract is from the Experimental Biology 2018 Meeting. There is no full text article associated with this abstract published in The FASEB Journal.