Imoxin attenuates LPS‐induced inflammation and MuRF1 expression in mouse skeletal muscle

Valentine, Rudy J.; Jefferson, Matthew; Kohut, Marian L.; Eo, Hyeyoon

doi:10.14814/phy2.13941

Cited by 22 publications

(18 citation statements)

References 59 publications

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“…All experiments were performed on animals of 4 months of age. In the LPS-induced inflammatory model, muscle inflammation induced was performed a described previously [54], except that 15 µg/kg of GW501516 was injected subcutaneously 2 h and 24 h prior LPS injection. In the carrageenan-induced inflammatory model, carrageenan solution (3%) at 10 mg/kg body weight was injected into the hindlimb muscle.…”

Section: Animal Experimentsmentioning

confidence: 99%

PPARβ/δ Agonism Upregulates Forkhead Box A2 to Reduce Inflammation in C2C12 Myoblasts and in Skeletal Muscle

Phua

Tan

Yip

et al. 2020

IJMS

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Daily activities expose muscles to innumerable impacts, causing accumulated tissue damage and inflammation that impairs muscle recovery and function, yet the mechanism modulating the inflammatory response in muscles remains unclear. Our study suggests that Forkhead box A2 (FoxA2), a pioneer transcription factor, has a predominant role in the inflammatory response during skeletal muscle injury. FoxA2 expression in skeletal muscle is upregulated by fatty acids and peroxisome proliferator-activated receptors (PPARs) but is refractory to insulin and glucocorticoids. Using PPARβ/δ agonist GW501516 upregulates FoxA2, which in turn, attenuates the production of proinflammatory cytokines and reduces the infiltration of CD45+ immune cells in two mouse models of muscle inflammation, systemic LPS and intramuscular injection of carrageenan, which mimic localized exercise-induced inflammation. This reduced local inflammatory response limits tissue damage and restores muscle tetanic contraction. In line with these results, a deficiency in either PPARβ/δ or FoxA2 diminishes the action of the PPARβ/δ agonist GW501516 to suppress an aggravated inflammatory response. Our study suggests that FoxA2 in skeletal muscle helps maintain homeostasis, acting as a gatekeeper to maintain key inflammation parameters at the desired level upon injury. Therefore, it is conceivable that certain myositis disorders or other forms of painful musculoskeletal diseases may benefit from approaches that increase FoxA2 activity in skeletal muscle.

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Section: Animal Experimentsmentioning

confidence: 99%

PPARβ/δ Agonism Upregulates Forkhead Box A2 to Reduce Inflammation in C2C12 Myoblasts and in Skeletal Muscle

Phua

Tan

Yip

et al. 2020

IJMS

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“…Immediately after decapitation, the gastrocnemius was extracted and flash-frozen with liquid nitrogen then stored at −80°C until the time of analysis. Western blot analysis followed previously described methods (Valentine et al, 2018 ). Approximately 15–25 μg of protein were separated by 4–15% gradient Stain-Free Criterion TGX gel electrophoresis (Bio-Rad, Hercules, CA, USA), and transferred onto a polyvinylidene difluoride membrane (MilliporeSigma, Burlington, MA, USA).…”

Section: Methodsmentioning

confidence: 99%

The Influence of Moderate Physical Activity on Brain Monoaminergic Responses to Binge-Patterned Alcohol Ingestion in Female Mice

Buhr

Reed

Shoeman

et al. 2021

Front. Behav. Neurosci.

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Monoamine neurotransmitter activity in brain reward, limbic, and motor areas play key roles in the motivation to misuse alcohol and can become modified by exercise in a manner that may affect alcohol craving. This study investigated the influence of daily moderate physical activity on monoamine-related neurochemical concentrations across the mouse brain in response to high volume ethanol ingestion. Adult female C57BL/6J mice were housed with or without 2.5 h of daily access to running wheels for 30 days. On the last 5 days, mice participated in the voluntary binge-like ethanol drinking procedure, “Drinking in the dark” (DID). Mice were sampled immediately following the final episode of DID. Monoamine-related neurochemical concentrations were measured across brain regions comprising reward, limbic, and motor circuits using ultra High-Performance Liquid Chromatography (UHPLC). The results suggest that physical activity status did not influence ethanol ingestion during DID. Moreover, daily running wheel access only mildly influenced alcohol-related norepinephrine concentrations in the hypothalamus and prefrontal cortex, as well as serotonin turnover in the hippocampus. However, access to alcohol during DID eliminated wheel running-related decreases of norepinephrine, serotonin, and 5-HIAA content in the hypothalamus, but also to a lesser extent for norepinephrine in the hippocampus and caudal cortical areas. Finally, alcohol access increased serotonin and dopamine-related neurochemical turnover in the striatum and brainstem areas, regardless of physical activity status. Together, these data provide a relatively thorough assessment of monoamine-related neurochemical levels across the brain in response to voluntary binge-patterned ethanol drinking, but also adds to a growing body of research questioning the utility of moderate physical activity as an intervention to curb alcohol abuse.

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“…We also found that Aspirin significantly inhibited the expression of autophagy-related proteins PINK1, BNIP3, LC3B and ATG7 in denervated skeletal muscle, suggesting that Aspirin inhibited the activity of autophagy lysosomal hydrolysis system. Studies have shown that inflammation can activate the expression of E3 ubiquitin ligases MuRF-1 and MAFbx (28,29). We found that the expression of inflammatory factors IL-6, IL-1 β and TNF-α in denervated skeletal muscle was significantly increased.…”

Section: Discussionmentioning

confidence: 64%

Aspirin alleviates denervation-induced muscle atrophy via regulating the Sirt1/PGC-1α axis and STAT3 signaling

Wan¹,

Zhang²,

Huang³

et al. 2020

Ann Transl Med

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Background: Our prior studies have shown that inflammation may play an important triggering role during the process of denervated muscle atrophy. The nonsteroidal anti-inflammatory drug aspirin exhibits the effect of anti-inflammatory factors. This study will investigate the protective effect of aspirin on denervated muscle atrophy and the underlying mechanism.Methods: Mouse models of denervated muscle atrophy were established. The protective effect of aspirin (20 mg/kg/d, i.p.) on denervated muscle atrophy was analyzed using the wet weight ratio of tibialis anterior (TA) muscle and muscle fiber cross-sectional area (CSA). The levels of inflammatory factors were detected using quantitative reverse transcription-polymerase chain reaction and enzyme-linked immunosorbent assay. Sirtuins1 (SIRT1)/Peroxisome Proliferator-Activated Receptor γ Co-Activator 1α (PGC-1α) and Signal transducer and activator of transcription 3 (STAT3) signaling pathway and the muscle fiber type related proteins in TA muscle after denervation were analyzed by western blot assay.Results: Intraperitoneal injection of aspirin (20 mg/kg/d) effectively alleviated denervation-induced muscle atrophy. This mainly manifested as follows: The wet weight ratio of TA muscle and muscle fiber CSA of mice treated with aspirin were significantly greater compared with mice treated with normal saline. The level of myosin heavy chain (MHC) increased, and the levels of muscle specific E3 ubiquitin ligase Muscle-specific RING finger-1 (MuRF-1) and muscle atrophy F-box (MAFbx) were decreased. Mitochondrial vacuolation and autophagy were inhibited, as evidenced by reduced level of autophagy related proteins PINK1, BNIP3, LC3B and Atg7 in mice treated with aspirin compared with mice treated with saline. In addition, aspirin treatment inhibited the slow-to-fast twitch muscle fiber conversion, which were related with triggering the expression of Sirt1 and PGC-1α. Moreover, aspirin reduced the levels of inflammatory factors interleukin-6, interleukin-1β and tumor necrosis factor-α and decreased the activation of STAT3 signaling pathway.Conclusions: This is the first study to find that aspirin can alleviate denervation-induced muscle atrophy and inhibit the type I-to-type II muscle fiber conversion and mitophagy possibly through regulating the STAT3 inflammatory signaling pathway and Sirt1/PGC-1α signal axis. This study expands our knowledge

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Imoxin attenuates LPS‐induced inflammation and MuRF1 expression in mouse skeletal muscle

Cited by 22 publications

References 59 publications

PPARβ/δ Agonism Upregulates Forkhead Box A2 to Reduce Inflammation in C2C12 Myoblasts and in Skeletal Muscle

PPARβ/δ Agonism Upregulates Forkhead Box A2 to Reduce Inflammation in C2C12 Myoblasts and in Skeletal Muscle

The Influence of Moderate Physical Activity on Brain Monoaminergic Responses to Binge-Patterned Alcohol Ingestion in Female Mice

Aspirin alleviates denervation-induced muscle atrophy via regulating the Sirt1/PGC-1α axis and STAT3 signaling

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