High-altitude hypoxia triggers JNK phosphorylation: the molecular switch linking hippocampal energy crisis, neuronal senescence and cognitive impairment

This dataset supports the study of "Chronic high-altitude hypoxia drives cognitive impairment, mitochondrial dysfunction, and cellular aging by activating the hippocampal JNK-P53 axis". Samples were collected at multiple time points using a chronic low-pressure hypoxia rat model (simulating an altitude of 6000 m), and the data included: (1) Western blot detection of protein expression and phosphorylation levels such as JNK/p53/Bim; (2) LC-MS/MS untargeted metabolomics analysis; (3) Immunofluorescence staining (LAMP1/Cox IV and PHD2/HIF-2 α); (4) Observation of transmission electron microscopy ultrastructure; (5) Morris water maze spatial memory test; (6) Morphological analysis of hippocampal CA1 region using HE staining. Statistical analysis was conducted using GraphPad Prism 10.1 for multiple sample comparisons (t-test/U-test/ANOVA/Kruskal Wallis et al.), while metabolomics was processed using MSDIAL 4.9 and differential metabolites were screened using Wilcoxon/ANOVA combined with VIP>1 and FC ≥ 1.5 (FDR corrected p<0.05). The dataset is shared using CC BY 4.0 protocol.