Short-term Dietary Selenium Deficiency Induced Liver Fibrosis by Inhibiting the Akt/mTOR Signaling Pathway in Rats.

The effects of short-term dietary selenium deficiency on the liver and protein kinase B (Akt)/mammalian target of rapamycin (mTOR) signaling pathway were evaluated. Fourteen growing rats were randomly divided into control and selenium deficiency groups and fed standard and selenium-deficient diets for 4 weeks, respectively. The serum and liver selenium concentrations were measured to evaluate the construction of animal models with selenium deficiency. Liver tissues were analyzed by transmission electron microscope, hematoxylin-eosin staining, and Masson staining to observe the ultrastructural changes, pathological changes, and severity of liver fibrosis, respectively. Besides, immunohistochemical staining (IHC) was used to analyze the effects of selenium deficiency on the expression of key proteins in the Akt/mTOR signaling pathway. The results showed that selenium concentrations in the serum and liver tissue were significantly lower in the selenium deficiency group than in the control group, and the selenium deficiency intervention could affect the morphology and structure of hepatocytes and mitochondria. Meanwhile, the liver tissue showed structural damage and fibrotic changes in the selenium deficiency group. The IHC results showed the positive staining rates of Akt, phosphorylation-modified protein kinase B (p-Akt), mTOR, and phosphorylation-modified mammalian target of the rapamycin (p-mTOR) in the liver of the selenium deficiency group which were significantly lower than that of the control group. In conclusion, short-term selenium deficiency dietary intervention could lead to liver fibrosis by inhibiting the Akt/mTOR signaling pathway.