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Baicalin is a natural flavonoid that has anti-apoptotic and anti-inflammatory effects. It shows some beneficial effects on muscle atrophy. However, its effects on age-related muscle atrophy are poorly understood. In this paper, we investigated whether baicalin exerts protective effect against skeletal muscle atrophy and its underlying mechanisms in aged mice using the grip strength test, histological analysis, and Western blots. Baicalin increased total muscle mass and strength in aged mice. Consistently, the cross-sectional area of quadriceps (QD) muscle significantly increased in both baicalin-administrated groups. Moreover, baicalin induced a shift in muscle fiber size distribution toward large fibers in both groups of mice. Expression levels of muscle atrophic factors, such as myostatin (MSTN) and atrogin-1, as well as pro-inflammatory cytokines, including tumor necrosis factor-alpha (TNF-α) and interleukin-6 (IL-6), were elevated in aged mice, but these increases were reduced by baicalin. While mitochondrial fission regulator, dynamin-related protein 1 (DRP-1), and apoptosis-related protein (apoptotic protease activating factor 1 (Apaf-1)) expressions were higher in aged mice than young mice, and their expression were downregulated following baicalin administration. The comprehensive results of this study suggest that baicalin provides beneficial effects on the treatment of sarcopenia not only by suppressing muscle atrophic factor expression and inflammation but also attenuating DRP-1-mediated mitochondrial fission and apoptosis.
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http://dx.doi.org/10.3390/muscles4030035 | DOI Listing |
JCI Insight
September 2025
Diabetes & Metabolism Research Center, University of Utah, Salt Lake City, United States of America.
Impaired muscle regrowth in aging is underpinned by reduced pro-inflammatory macrophage function and subsequently impaired muscle cellular remodeling. Macrophage phenotype is metabolically controlled through TCA intermediate accumulation and activation of HIF1A. We hypothesized that transient hypoxia following disuse in old mice would enhance macrophage metabolic inflammatory function thereby improving muscle cellular remodeling and recovery.
View Article and Find Full Text PDFMetabolomics
September 2025
Department of Biochemistry, University of Oxford, South Parks Road, Oxford, OX1 3QU, UK.
Introduction: Knockout of the Fmo5 gene in mice led to a lean, slow-ageing phenotype characterised by the presence of 2,3-butanediol isomers in their urine and plasma. Oral treatment of wildtype mice with 2,3-butanediol led to a low cholesterol, low epididymal fat phenotype.
Objectives: Determine if significant, heterozygous coding variations in human FMO5 would give rise to similar clinical and metabolic phenotypes in humans, as in C57BL/6J mice with knockout of the Fmo5 gene and in particular, increased excretion of 2,3-butanediol.
Elife
September 2025
Department of Neuroscience, Washington University School of Medicine, St Louis, United States.
Peripheral sensory neurons regenerate their axons after injury to regain function, but this ability declines with age. The mechanisms behind this decline are not fully understood. While excessive production of endothelin 1 (ET-1), a potent vasoconstrictor, is linked to many diseases that increase with age, the role of ET-1 and its receptors in axon regeneration is unknown.
View Article and Find Full Text PDFFASEB J
September 2025
Department of Surgery, McMaster University, Hamilton, Ontario, Canada.
Severe burns are a major global health concern, and are associated with long-term physical and psychological impairments, multi-organ dysfunction, and substantial morbidity and mortality. While burn injuries in adults trigger systemic immuno-metabolic alterations-characterized by white adipose tissue browning, elevated resting energy expenditure, widespread catabolism, and inflammation-these adaptive responses are considerably impaired in older adults, with molecular mechanisms behind these differences remaining largely unclear. As a key regulator of systemic metabolism, investigating the pathological role of adipose tissue (AT) postburn may reveal novel targets that could potentially improve patient outcomes.
View Article and Find Full Text PDFJCI Insight
September 2025
Division of Cardiovascular Medicine, Department of Medicine.
Aortic valve stenosis is a progressive and increasingly prevalent disease in older adults, with no approved pharmacologic therapies to prevent or slow its progression. Although genetic risk factors have been identified, the contribution of epigenetic regulation remains poorly understood. Here, we demonstrated that histone deacetylase 3 (HDAC3) maintains aortic valve structure by suppressing mitochondrial biogenesis and preserving extracellular matrix integrity in valvular interstitial fibroblasts.
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