生物能量学：开放获取

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Altered Hepcidin Expression is Part of the Choroid Plexus Response to IL-6/Stat3 Signaling Pathway in Normal Aging Rats

Chongbin L, Rui W, Chunyan W, Chen HU and Qifeng D

Accumulating evidence has revealed that brain iron concentrations increase with aging, and the choroid plexus may be at the basis of iron-mediated toxicity and the increase in inflammation and oxidative stress that occurs with aging. However, nothing is known concerning the correlation between the IL-6/Stat3 signaling pathway and the levels of hepcidin expression at the choroid plexus (CP) in normal aging. The morphological modifications as a function of aging were investigated and the present study used quantitative real time PCR (qPCR) and western blotting (WB) to determine the alterations in specific mRNA and corresponding protein changes at the CP on aging at ages 3, 6, 9, 12, 15, 18, 21, 24, 27, 30, 33 and 36 m Brown-Norway/Fischer (B-N/F) rats. Results showed that a striking deterioration of the CP epithelial cells, and results also firstly demonstrated that hepcidin expression at the choroid plexus increased with aging at the mRNA level and might cause corresponding changes in protein expression. These alterations in normal aging were in accordance with the expression and secretion of IL-6 and Stat3. Our data suggest that IL-6 regulate hepcidin expression at the choroid plexus, upon interaction with the cognate cellular receptor, and through the Stat3 signaling transduction pathway. The enhanced Stat3 signaling responsiveness to proinflammatory factors may impact on mechanisms of Alzheimer’s disease.