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Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction [C2C12]

ABSTRACT: Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction [C2C12]

PROVIDER: PRJNA945399 | ENA |

REPOSITORIES: ENA

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Jakyak-gamcho-tang ameliorates dexamethasone (DEX)-induced muscle atrophy and muscle dysfunction [Gastrocnemius and Soleus]

Project description:Jakyak-gamcho-tang (JGT) is a herbal medicine that has been traditionally prescrived for pain control including muscular pain. Muscle atrophy is a disease that is characterized with a gradual muscle loss. Muscle atrophy is clearly observed in experimental animals that receive a repeated high-dose of an artificial glucocorticoid, dexamethasone (DEX). This transcriptome analysis aims to investigate the changes in global gene expression profiles in gastrocnemius (GA) and soleus (SO) muscle tissues from mice with DEX-induced muscle atrophy in the presence or absence of JGT co-treatment.

2023-03-21 | GSE227495 | GEO

Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction [C2C12]

Project description:Jakyak-gamcho-tang (JGT) is a herbal medicine that has been traditionally prescrived for pain control including muscular pain. This transcriptome analysis aims to investigate the changes in global gene expression profile in differentiated murine C2C12 myotube cells treated with JGT extract.

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Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction

Project description:Jakyak-gamcho-tang ameliorates dexamethasone-induced muscle atrophy and muscle dysfunction

| PRJNA945385 | ENA

Jakyak-gamcho-tang ameliorates dexamethasone (DEX)-induced muscle atrophy and muscle dysfunction [Gastrocnemius and Soleus]

Project description:Jakyak-gamcho-tang ameliorates dexamethasone (DEX)-induced muscle atrophy and muscle dysfunction [Gastrocnemius and Soleus]

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Induction of muscle atrophy by tumor and dexamethasone regulates a distinct set of proteins from atrophy caused by aging

Project description:To assess changes in the muscle proteome that due to tumor burden and dexamethasone treatments and compare proteomic changes that occur in atrophy due to tumor burden and dexamethasone treatment with atrophy caused by aging. Regulators of muscle atrophy induced by diseases such as cancer or drugs such as dexamethasone are largely unknown. We would therefore like to determine the proteomic signature of atrophying muscle caused by tumor burden (LLC cell injected mice) and dexamethasone treatment in order to examine possible biomarkers and regulators of muscle atrophy. We would also like to compared the proteomic signature of different modes of muscle atrophy to determine similarities and differences in the possible biomarkers and regulators.

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Effect of Actn3 genotype on dexamethasone response in skeletal muscle

Project description:To examine the effect of alpha-actinin-3 deficiency on muscle atrophy response following dexamethasone treatment.

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Genome-wide analysis of dexamethasone-responsive gene expression in mouse triceps surae muscle

Project description:Analysis of dexamethasone-regulation of muscle mass at gene expression level. The hypothesis tested in the present study was that the presence of MuRF1 contributes to the extent of gene expression changes observed in specific sets of genes during a challenge leading to muscle atrophy. Results provide important information on the response of triceps surae muscle to synthetic glucocorticoid treatment, such as specific cell signaling and metabolic enzyme genes, that may be influenced by MuRF1 during atrophy. Total RNA obtained from isolated triceps surae muscle subjected to 3 or 14 days dexamethasone treatment compated to untreated littermate control muscles.

2013-02-12 | E-GEOD-44208 | biostudies-arrayexpress

Expression data from tibialis anterior muscle of mice with or without treatment of dexamethasone and/or tumeric extract

Project description:Sarcopenia is the decline in skeletal muscle mass, strength, and functions, which decreases the quality of life in elderly people. This study investigated the suppressive effect of turmeric (Curcuma longa) extract (TE) on muscle atrophy in dexamethasone (DEX)-treated mice and C2C12 myotubes. DEX treatment significantly decreased the muscle weight and significantly increased Fbxo32 and Murf1 expression in mice, and these changes were suppressed by the supplementation of an AIN-93 based diet with 2% TE. A similar pattern was observed in FBXO32 and MuRF1 protein expression. In C2C12 myotubes, DEX treatment significantly increased FBXO32 and MuRF1 gene and protein expression, and these increases were significantly suppressed by TE supplementation at a concentration of 200 µg/ml. Furthermore, one of the five TE fractions, which were separated by high-performance liquid chromatography had a similar effect with TE supplementation. The present study proposes the suppressive effect of turmeric on sarcopenia.

2022-07-23 | GSE209528 | GEO

Genome-wide analysis of dexamethasone-responsive gene expression in mouse triceps surae muscle

2013-02-12 | GSE44208 | GEO

NLRP3 inflammasome activation aggravates skeletal muscle atrophy in experimental model of denervation

Project description:The innervation of skeletal myofibers exerts a crucial influence on the maintenance of muscle tone and normal operation, but little is known concerning atrophy and its underlying mechanisms in denervated muscle to date. Here, we reported that activated NOD-like receptor protein 3 (NLRP3) inflammasome with pyroptotic cell death occurred in denervated gastrocnemius in the mouse model of sciatic denervation. This damage causes interleukin 1 beta (IL-1β) release，facilitating the ubiquitin proteasome system (UPS) activation, which was responsible for muscle proteolysis. Conversely, genetic knock-out of muscular NLRP3 inhibited the pyroptosis-associated protein expression and ameliorate muscle atrophy significantly. Meanwhile, co-treatment with shRNA-NLRP3, also remarkably attenuated NLRP3 inflammasome activator (NIA)-induced C2C12 myotube pyroptosis and atrophy. Interestingly, we also observed a correlation between NLRP3 inflammasome activation and muscular apoptosis possibly via caspase 1 mediation after denervation. This work for the first time elucidates on the roles and mechanisms of NLRP3 inflammasome in skeletal muscle atrophy during denervation and suggests the potential contribution to the pathogenesis of neuromuscular diseases.

2022-12-29 | GSE201133 | GEO

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