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Ghrelin is a gut hormone shown to have protective effects throughout the gastrointestinal tract. This study aims to investigate its protective effect in celiac disease induced in rats. Twenty-four rat pups were divided into 4 groups as follows: control, disease (1.5 mg/g intragastric gliadin), co-treatment (50 ng/g intraperitoneal ghrelin after gliadin gavage) and pretreatment (50 ng/g intraperitoneal ghrelin before gliadin gavage). Animals’ weight gain was charted. Histological features assessed include villus length, villus width, crypt depth and number of intraepithelial lymphocytes. Tissue interferon-gamma was quantified by ELISA. ANOVA was used to compare results statistically. Results showed that villi were shortened in the diseased group, but were as long as the control in pretreatment and co-treatment groups. Crypt depth had increased in disease group, but turned to normal in co-treatment group. Number of intraepithelial lymphocytes was significantly higher in disease group than the control, while no difference was observed between co-treatment and control groups. Disease and control animals weighed equally at the end of the experiment, but ghrelin-treated animals had significantly gained more weight than these two. Interferon-gamma measurement revealed no significant difference among groups. We concluded administration of ghrelin led to histological improvement of celiac disease which was more obvious if administered after exposure to gliadin.

Endoplasmic reticulum (ER) stress provides abnormalities in insulin action, inflammatory responses, lipoprotein B100 degradation and hepatic lipogenesis. Excess accumulation of triglyceride in hepatocytes may also lead to disorders such as non-alcoholic fatty liver disease (NAFLD) and nonalcoholic steatohepatitis (NASH). Opioid peptides are involved in triglyceride and cholesterol dysregulation, inflammation and cell death. In this study, we evaluated Naltrexone effects on ER stress induced liver injury. To do so, C57/BL6 mice received saline, DMSO and Naltrexone, as control groups. ER stress was induced by tunicamycin (TM) injection. Naltrexone was given before TM administration. Liver blood flow and biochemical serum analysis were measured. Histopathological evaluations, TNF-α measurement and Real-time RT-PCR were also performed. TM challenge provokes steatosis, cellular ballooning and lobular inflammation which significantly reduced in Naltrexone treated animals. ALT, AST and TNF-α increased in the TM group and improved in the Naltrexone plus TM group. Triglyceride and cholesterol levels decreased in TM treated mice with no increase in Naltrexone treated animals. In the Naltrexone plus TM group, gene expression of Bax/Bcl-2 ratio and caspase3 significantly lowered compared with the TM group. In this study, we found that Naltrexone had a notable alleviating role in ER stress induced steatosis and liver injury.