Article data - AGING MODEL IMPAIRS MEMORY, MOTOR FUNCTION, AND TRIGGERS INFLAMMATION AND OXIDATIVE STRESS IN RATS
Description
Chronic D-galactose (D-GAL) administration is a well-established model of accelerated aging that reproduces several physiological alterations associated with natural aging, including oxidative stress, neuroinflammation, mitochondrial dysfunction, and cognitive decline. This dataset was generated to test the hypothesis that chronic D-GAL administration impairs aerobic capacity and recognition memory while increasing oxidative stress and disrupting inflammatory homeostasis in the brain and skeletal muscles. Thirty male Wistar rats were randomly assigned to Control (CON, n = 15) or D-GAL (150 mg·kg⁻¹·day⁻¹, intraperitoneally for 8 weeks; n = 15) groups. Before and after treatment, animals underwent behavioral and physical evaluations, including the Novel Object Recognition (NOR) test for short- and long-term memory, the Maximal Weight Carried (MWC) test for muscle strength, and an incremental treadmill test to determine aerobic capacity, VO₂peak, and mechanical work. Forty-eight hours after the experimental protocol, the hippocampus, frontal cortex, soleus, and extensor digitorum longus (EDL) muscles were collected for biochemical analyses. The dataset contains raw individual measurements of body mass, cognitive performance, muscle strength, aerobic capacity, oxidative stress biomarkers (TBARS and hydroperoxides), protein concentration, and inflammatory cytokines (IL-1β, IL-6, TNF-α, and IL-10) quantified by ELISA in the hippocampus, frontal cortex, soleus, and EDL muscles. Raw data are provided for each animal, allowing independent statistical analyses, verification of published results, and secondary analyses. The data demonstrate that chronic D-GAL administration induced an accelerated aging phenotype characterized by reduced aerobic capacity, lower VO₂peak, decreased mechanical work, and impaired long-term recognition memory. Oxidative stress increased, as indicated by elevated hydroperoxide concentrations in the hippocampus and EDL muscle and increased TBARS levels in the hippocampus. The most consistent inflammatory alteration was a reduction in the anti-inflammatory cytokine IL-10 in the hippocampus, frontal cortex, and soleus muscle, whereas no significant changes were observed for IL-1β, IL-6, or TNF-α. This dataset integrates behavioral, physiological, and biochemical outcomes obtained from the same animals, enabling correlation analyses between functional performance and molecular biomarkers. It provides a valuable resource for studies on experimental aging, neurodegeneration, sarcopenia, oxidative stress, inflammation, exercise physiology, and age-related cognitive decline, as well as for reproducibility studies, systematic reviews, and future meta-analyses.
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Institutions
- Universidade Federal de Minas GeraisMinas Gerais, Belo Horizonte