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Dietary habits can alter the skeletal muscle performance and mass, and Undaria pinnatifida extracts are considered a potent candidate for improving the muscle mass and function. Therefore, in this study, we aimed to assess the effect of U pinnatifida extracts on exercise endurance and skeletal muscle mass. C57BL/6 mice were fed a 0.25% U pinnatifida extract‐containing diet for 8 weeks. U pinnatifida extract‐fed mice showed increased running distance, total running time, and extensor digitorum longus and gastrocnemius muscle weights. U pinnatifida extract supplementation upregulated the expression of myocyte enhancer factor 2C, oxidative muscle fiber markers such as myosin heavy chain 1 (MHC1), and oxidative biomarkers in the gastrocnemius muscles. Compared to the controls, U pinnatifida extract‐fed mice showed larger mitochondria and increased gene and protein expression of molecules involved in mitochondrial biogenesis and oxidative phosphorylation, including nuclear respiratory factor 2 and mitochondrial transcription factor A. U pinnatifida extract supplementation also increased the mRNA expression of angiogenesis markers, including VEGFa, VEGFb, FGF1, angiopoietin 1, and angiopoietin 2, in the gastrocnemius muscles. Importantly, U pinnatifida extracts upregulated the estrogen‐related receptor γ and peroxisome proliferator‐activated receptor gamma co‐activator 1‐alpha (PGC‐1α)/AMP‐activated protein kinase (AMPK)/sirtuin 1 (SIRT1) networks, which are partially increased by fucoxanthin, hesperetin, and caffeic acid treatments. Collectively, U pinnatifida extracts enhance mitochondrial biogenesis, increase oxidative muscle fiber, and promote angiogenesis in skeletal muscles, resulting in improved exercise capacity and skeletal muscle mass. These effects are attributable to fucoxanthin, hesperetin, and caffeic acid, bioactive components of U pinnatifida extracts. [ABSTRACT FROM AUTHOR]

• Codium fragile (CF) is a green algae with unknown effects on skeletal muscle. • Canthaxanthin is a new compound found in CF in the present study. • In mice fed with a CF extract, exercise endurance and muscle weight increased. • CF promoted protein expression and myogenic differentiation via the mTORC1. • Canthaxanthin partially contributes to the efficacy of CF in skeletal muscle. Codium fragile (CF) is a type of green algae consumed as kimchi in Asia. UPLC-QTOF-MS/MS analysis showed that CF contain lysophosphatidyl choline, canthaxanthin, retinoic acid, α-tocopherol, and unsaturated fatty acids, which reportedly improve skeletal muscle health. However, the effect of CF on skeletal muscle mass and function remains to be elucidated. In mice fed with CF extracts, exercise endurance and muscle weight increased. CF extracts enhanced protein synthesis and myogenic differentiation through the mTORC1 pathway. CF extracts also promoted oxidative muscle fiber formation and mitochondrial biogenesis through the PGC-1α-related signaling pathway. Upregulation of PGC-1α by CF extracts was abolished by EX527 SIRT1 inhibitor treatment. Changed signaling molecules in the CF extracts were partially regulated by canthaxanthin, a new compound in CF extracts, suggesting that canthaxanthin contribute synergistically to the effect of CF extracts. Therefore, CF is a potential food source for sport nutrition or prevention of sarcopenia. [ABSTRACT FROM AUTHOR]

The widespread prevalence of micro and nanoplastics in the environment raises concerns about their potential impact on human health. Recent evidence demonstrates the presence of nanoplastics in human blood and tissues following ingestion and inhalation, yet the specific risks and mechanisms of nanoplastic toxicity remain inadequately understood. In this study, we aimed to explore the molecular mechanisms underlying the toxicity of nanoplastics at both systemic and molecular levels by analyzing the transcriptomic/metabolomic responses and signaling pathways in the intestines of mice after oral administration of nanoplastics. Transcriptome analysis in nanoplastic-administered mice revealed a notable upregulation of genes involved in pro-inflammatory immune responses. In addition, nanoplastics substantially reduced the expression of tight junction proteins, including occludin, zonula occluden-1, and tricellulin, which are crucial for maintaining gut barrier integrity and function. Importantly, nanoplastic administration increased gut permeability and exacerbated dextran sulfate sodium-induced colitis. Further investigation into the underlying molecular mechanisms highlighted significant activation of signaling transsducer and activator of transcription (STAT)1 and STAT6 by nanoplastic administration, which was in line with the elevation of interferon and JAK-STAT pathway signatures identified through transcriptome enrichment analysis. Additionally, the consumption of nanoplastics specifically induced nuclear factor kappa-B (NF-κB) and extracellular signal-regulated kinase (ERK)1/2 signaling pathways in the intestines. Collectively, this study identifies molecular mechanisms contributing to adverse effects mediated by nanoplastics in the intestine, providing novel insights into the pathophysiological consequences of nanoplastic exposure. [Display omitted] • Ingesting polystyrene nanoplastics (NPs) exacerbates DSS-induced colitis in vivo. • Transcriptomic analysis reveals that NPs induce pro-inflammatory gene expression. • NPs induce metabolomic alterations, such as depletion of taurine in the mouse colon. • NPs induce inflammation via JAK-STAT and ERK1/2 signaling pathways. • NPs reduce expression of tight junction proteins and compromise gut barrier function. [ABSTRACT FROM AUTHOR]

To develop an effective treatment for muscle recovery, costimuli effect of cyclic stretch and hypoxia on the recovery of oxidative damaged skeletal muscle cells is investigated. C2C12 myoblast cells are differentiated into myotube in culture dish followed by seeding the myotubes in the microfluidic device for further growth. Hydrogen peroxide is used to induce oxidative stress on myotubes for mimicking intracellular muscle damage. Afterward, the damaged myotubes are recovered in either normoxia or hypoxia environment with or without cyclic stretch, to elucidate the effect of the stretch and hypoxia on recovery. For analysis, reactive oxygen species, 8‐hydroxydeoxyguanosine, and myosin heavy chain are chosen as recovery indicators and it is shown that cyclic stretch and hypoxia facilitate the recovery of muscle to the greatest extent when both cyclic stretch and hypoxia are applied. To investigate the mechanism of the stretch and hypoxia intervened recovery, hypoxia inducible factor‐1α (HIF‐1α), peroxiredoxin 2, glutathione peroxidase 1, and catalase are selected as candidates for the key factor of recovery acceleration. There is evidence that HIF‐1α and antioxidants contributed to stretch‐/hypoxia‐induced recovery, and HIF‐1α is speculated to play the most important role. Hence, the stretch and hypoxia triggered pathways of cellular recovery are suggested. [ABSTRACT FROM AUTHOR]

Investigation on the Effect of Cyclic Stretch and Hypoxia on Recovery of Damaged Skeletal Muscle Cells Using Microfluidic System (Adv. Keywords: microfluidic chip; damage model of myotube; cyclic stretch; hypoxia; hypoxia inducible factor-1 EN microfluidic chip damage model of myotube cyclic stretch hypoxia hypoxia inducible factor-1 1 1 1 11/09/21 20211101 NES 211101 B Increased Recovery Rate of Damaged Muscle b Hyung-Soon Park, Jessie S. John, and colleagues demonstrate how the combination of cyclic stretch and hypoxic conditions leads to an increased recovery rate of damaged muscle in article numer 2100465, by activating the reactive oxygen species recovery-related pathways as found in the microfluidic-based muscle damage model. Microfluidic chip, damage model of myotube, cyclic stretch, hypoxia, hypoxia inducible factor-1. [Extracted from the article]