高原环境会导致机体缺氧引起高原反应，而促使血红蛋白增多可有效缓解组织低氧。机体铁代谢变化对血红蛋白合成有重要影响，因此阐明低氧下影响机体铁代谢变化的因素和分子机制，可为采取措施增加高原低氧下血红蛋白含量提供重要依据。饥饿素（Ghrelin）是全身循环性激素，在中枢和外周具有多种生物学功能。研究发现常氧下Ghrelin可通过GHSR1a/MAPK信号通路上调铁输出蛋白1（Fpn1）的表达促进铁释放，进而影响机体的铁代谢。本研究假设低压低氧下可通过提高Ghrelin含量来激活Ghrelin/GHSR1a/MAPK信号通路，上调Fpn1表达增加组织铁输出，从而提高血清铁含量加速机体铁动员，最终达到为红细胞合成提供更多铁元素，使机体更快更好适应高原低氧环境的目的。本研究拟从在体和离体水平探讨高原低氧下Ghrelin对机体铁代谢的影响及其分子机制，为防治高原反应对机体功能影响提供新的思路。

Plateau environment can cause tissue hypoxia and further trigger the plateau reaction in human. Increasing of hemoglobin can effectively alleviate the hypoxic reaction under plateau hypoxia. The change of iron metabolism has an important influence on hemoglobin synthesis. Therefore, elucidating the factors and molecular mechanisms involved in iron metabolism under hypoxia can provide important evidence for exploring measures to promote hemoglobin increase. Ghrelin is a systemic circulatory hormone, which not only plays an important role in the central nervous system, but also in the peripheral system. It was found that Ghrelin can stimulate iron release by upregulating Ferroportin 1 (Fpn1) through GHSR1a/MAPK signaling pathway, and further affects iron metabolism. The previous study of our group confirmed that the contents of serum Ghrelin and serum iron were both decreased in plateau hypoxia. Therefore, we hypothesized that increased Ghrelin in plateau hypoxic condition may upregulate the expression of Fpn1 through activation of Ghrelin/GHSR1a/MAPK signaling pathway, and increase iron export, thereby increasing the serum iron content and accelerates the mobilization of body iron in response to hypoxia conditions. This study is trying to investigate the role of Ghrelin on iron metabolism and the molecular mechanism involved in this process at high altitude hypoxia both in vivo and in vitro. It may provide us a new strategy in prevention and cure of high altitude disease.