Hypoxic preconditioning (HPC) exerts a protective effect against hypoxic/ischemic brain injury, and one mechanism explaining this effect may involve the upregulation of hypoxia-inducible factor-1 (HIF-1). Autophagy, an endogenous protective mechanism against hypoxic/ischemic injury, is correlated with the activation of the HIF-1α/Beclin1 signaling pathway. Based on previous studies, we hypothesize that the protective role of HPC may involve autophagy occurring via activation of the HIF-1α/Beclin1 signaling pathway. To test this hypothesis, we evaluated the effects of HPC on oxygen-glucose deprivation/reperfusion (OGD/R)-induced apoptosis and autophagy in SH-SY5Y cells. HPC significantly attenuated OGD/R-induced apoptosis, and this effect was suppressed by the autophagy inhibitor 3-methyladenine and mimicked by the autophagy agonist rapamycin. In control SH-SY5Y cells, HPC upregulated the expression of HIF-1α and downstream molecules such as BNIP3 and Beclin1. Additionally, HPC increased the LC3-II/LC3-I ratio and decreased p62 levels. The increase in the LC3-II/LC3-I ratio was inhibited by the HIF-1α inhibitor YC-1 or by Beclin1-short hairpin RNA (shRNA). In OGD/R-treated SH-SY5Y cells, HPC also upregulated the expression levels of HIF-1α, BNIP3, and Beclin1, as well as the LC3-II/LC3-I ratio. Furthermore, YC-1 or Beclin1-shRNA attenuated the HPC-mediated cell viability in OGD/R-treated cells. Taken together, our results demonstrate that HPC protects SH-SY5Y cells against OGD/R via HIF-1α/Beclin1-regulated autophagy.

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Sodium chloride is a major source of salt in human nutrition. It is well-known that long-term high-salt diet (HSD) was associated with the development of hypertension and cardiovascular disease, especially when sodium intake exceeds 5 g/day. 1 There is an emerging evidence that the consumptions of dietary sodium are usually excess of requirements in the form of salt in many countries among adults and childrens, and then, leading to the excess weight gain. 2 Strikingly, both experimental data from animal and epidemiological data from clinical investigations in human being demonstrated that long-term HSD may cause cognitive dysfunction and brain tissue damage in adult individuals. 3,4 Data from rodents reported that HSD impaired cognitive function without changing blood pressure. 5,6 Furthermore, HSD disturbed the short-and long-term memory of mouse with corresponding increases in hippocampal oxidative stress and deregulation of synaptic protein/neurotrophin. 6 The importance of adequate maternal nutrition during the development for offspring's long-term physical health has

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