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The effects of ethanol extract of Bidens pilosa L. (EEB) on acute exercise fatigue and its underlying biochemical mechanism were investigated in this study. Sixty adult male ICR mice were divided into control, model, vitamin C (VC) 100, EEB40, EEB80, and EEB160 groups, receiving VC (100 mg/kg) or EEB (40, 80, 160 mg/kg) for 28 days (intragastrically, I.G.). The mice underwent tail- suspension, elevated plus maze (EPM), rotarod, and loaded swimming tasks and biochemical indices were measured. There were no significant differences in body weight, tail suspension time, EPM open arm time/entries and serum cortisone levels among the groups. Compared with the model group, there was an increase in rotarod latency in the VC100/EEB80 groups and an increase in loaded swimming time in the EEB80/EEB160 groups. Furthermore, the haptic and muscle glycogen levels decreased in the model group, while the haptic glycogen levels increased in the all VC/EEB groups. Similarly, the serum lactate and creatinine levels increased in the model group, but decreased in lactate (except for EEB 160), creatinine (except for EEB40) and lactate dehydrogenase in the EEB80 group. In the liver, malonaldehyde (MDA) and oxidized glutathione (GSSG) levels increased in the model group; however, glutathione reductase (GR) (except for EEB40), glutathione (GSH) and GSH/GSSG ratios increased, with GSSG levels decreasing in all VC/EEB groups. In the quadriceps, the GR levels increased in the model, whereas it decreased in the VC100, EEB40 and EEB80 groups. These results suggest that EEB has anti-acute fatigue effect, potentially attributed to mitigate metabolite accumulation, enhancing glycogen reserves, and fortifying the antioxidant mechanism. [ABSTRACT FROM AUTHOR]

Although studies have demonstrated that genome instability is accumulated in patients with Alzheimer's disease (AD), the specific types of genome instability linked to AD pathogenesis remain poorly understood. Here, we report the first characterization of the age‐ and sex‐related trajectories of telomere length (TL) and micronuclei in APP/PS1 mice model and wild‐type (WT) controls (C57BL/6). TL was measured in brain (prefrontal cortex, cerebellum, pituitary gland, and hippocampus), colon and skin, and MN was measured in bone marrow in 6‐ to 14‐month‐old mice. Variation in TL was attributable to tissue type, age, genotype and, to a lesser extent, sex. Compared to WT, APP/PS1 had a significantly shorter baseline TL across all examined tissues. TL was inversely associated with age in both genotypes and TL shortening was accelerated in brain of APP/PS1. Age‐related increase of micronuclei was observed in both genotypes but was accelerated in APP/PS1. We integrated TL and micronuclei data with data on cognition performance and brain amyloidosis. TL and micronuclei were linearly correlated with cognition performance or Aβ40 and Aβ42 levels in both genotypes but to a greater extent in APP/PS1. These associations in APP/PS1 mice were dominantly driven by females. Together, our findings provide foundational knowledge to infer the TL and micronuclei trajectories in APP/PS1 mice during disease progression, and strongly support that TL attrition and micronucleation are tightly associated with AD pathogenesis in a female‐biased manner. [ABSTRACT FROM AUTHOR]