Delphinidin prevents disuse muscle atrophy and reduces stress-related gene expression

Murata, Mariko; Kosaka, Reia; Kurihara, Kana; Yamashita, Shigeki; Tachibana, Hirofumi

doi:10.1080/09168451.2016.1184560

Cited by 16 publications

(23 citation statements)

References 25 publications

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“…Here we report a significant increase in the mRNA levels of Cbl-b in the soleus muscle of the unloaded animals that was completely prevented by allopurinol. Cbl-b-deficient mice are resistant to unloading-induced atrophy 11 and its inhibition with delphinidin (an anthocyanin), suppresses the atrophy of skeletal muscle in a rodent model of disuse 51 . IRS-1 is the docking protein for the regulatory subunit of PI-3K, the kinase that activates Akt.…”

Section: Discussionmentioning

confidence: 99%

Allopurinol partially prevents disuse muscle atrophy in mice and humans

Ferrando

Gómez-Cabrera

Salvador‐Pascual

et al. 2018

Sci Rep

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Disuse muscle wasting will likely affect everyone in his or her lifetime in response to pathologies such as joint immobilization, inactivity or bed rest. There are no good therapies to treat it. We previously found that allopurinol, a drug widely used to treat gout, protects muscle damage after exhaustive exercise and results in functional gains in old individuals. Thus, we decided to test its effect in the prevention of soleus muscle atrophy after two weeks of hindlimb unloading in mice, and lower leg immobilization following ankle sprain in humans (EudraCT: 2011-003541-17). Our results show that allopurinol partially protects against muscle atrophy in both mice and humans. The protective effect of allopurinol is similar to that of resistance exercise which is the best-known way to prevent muscle mass loss in disuse human models. We report that allopurinol protects against the loss of muscle mass by inhibiting the expression of ubiquitin ligases. Our results suggest that the ubiquitin-proteasome pathway is an appropriate therapeutic target to inhibit muscle wasting and emphasizes the role of allopurinol as a non-hormonal intervention to treat disuse muscle atrophy.

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Section: Discussionmentioning

confidence: 99%

Allopurinol partially prevents disuse muscle atrophy in mice and humans

Ferrando

Gómez-Cabrera

Salvador‐Pascual

et al. 2018

Sci Rep

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Section: Delphinidinmentioning

confidence: 99%

“…Delphinidin is found in pigmented fruits and vegetables and confers a blue-red color (Murata et al, 2016). Two studies have suggested that delphinidin prevents muscle atrophy by characterizing its underlying mechanisms (Murata et al, 2016;. Delphinidin significantly reversed MuRF1 expression by upregulating the nuclear factor of activated T cells 3 (NFATc3) and miR-23a (Murata et al, 2017).…”

Section: Delphinidinmentioning

confidence: 99%

“…These results suggest that the reduction of MuRF1 expression in response to delphinidin treatment is mediated by the NFATc3/miR-23a pathway but not by the Akt/FoxO pathway. Delphinidin also reduced the expression of Cbl-b or a RING-type ubiquitin ligase in dexamethasone-treated C2C12 myotubes (Murata et al, 2016). In particular, Murata et al (2017) compared cyanidin (3,3 0 ,4 0 ,5,7-pentahydroxyflavylium) and delphinidin (3,3 0 ,4 0 ,5,5 0 ,7-hexahydroxyflavylium) to investigate their effects on MuRF1 expression.…”

Section: Delphinidinmentioning

confidence: 99%

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Flavonoids: nutraceutical potential for counteracting muscle atrophy

Kim

Hwang

2020

Food Sci Biotechnol

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Skeletal muscle plays a vital role in the conversion of chemical energy into physical force. Muscle atrophy, characterized by a reduction in muscle mass, is a symptom of chronic disease (cachexia), aging (sarcopenia), and muscle disuse (inactivity). To date, several trials have been conducted to prevent and inhibit muscle atrophy development; however, few interventions are currently available for muscle atrophy. Recently, food ingredients, plant extracts, and phytochemicals have received attention as treatment sources to prevent muscle wasting. Flavonoids are bioactive polyphenol compounds found in foods and plants. They possess diverse biological activities, including anti-obesity, anti-diabetes, anti-cancer, anti-oxidation, and anti-inflammation. The effects of flavonoids on muscle atrophy have been investigated by monitoring molecular mechanisms involved in protein turnover, mitochondrial activity, and myogenesis. This review summarizes the reported effects of flavonoids on sarcopenia, cachexia, and disuse muscle atrophy, thus, providing an insight into the understanding of the associated molecular mechanisms.

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“…Previously, the increased expression of Nox4 was found in m. quadriceps femoris of 10-day tailsuspended mice [68].…”

Section: Discussionmentioning

confidence: 87%

TNFa is Involved in the Development of Disuse Muscle Atrophy Through the Acid Sphingomyelinase/ Ceramide Up-Regulation and Pro-Oxidant Signaling

Брындина

Ovchinina

Protopopov

et al. 2020

Preprint

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Background: There is paucity of data indicating the role of cytokines including TNFa in the development of disuse muscle atrophy, despite the growing interest to this problem emerging in the recent years. The aim of the present study was to test the hypothesis that TNFa/ TNFR1 may be involved in the development of disuse muscle atrophy caused by unloading through aSMase/ ceramide/ ROS mechanism. Methods: The experiments were performed on male Wistar rats (180 – 230g) subjected to 4 or 14 days of hindlimb suspension (HS) and treated with clomipramine (HS+Clom) or vehicle. The following parameters were studied: TNFR1, aSMase, nSMase and Nox2 proteins and ceramide in detergent-resistant membrane (DRM) fraction isolated from soleus muscle homogenates, pro-oxidant/anti-oxidant and pro-apoptotic/anti-apoptotic activities, immune fluorescence intensity and distribution of ceramide, Nox2, Nox4 and caveolin-3 on longitudinal and transverse muscle sections. The relative muscle mass, cross-sectional area (CSA) and Feret’s diameter (FD) of muscle fibers were used to confirm muscle atrophy. Statistical analysis was performed using one-way ANOVA followed by the Bonferroni post hoc test, or Cruskall-Wallis and Mann-Whitney U test. Results: Disuse caused an increase in membrane TNFR1, aSMase, ceramide abundance in DRM, up-regulation of pro-oxidant and pro-apoptotic capacities (increased Nox2, Nox4, TBA-active products, Bax/Bcl-2 ratio, elevated activity of caspase-3/7 and -6). The most of alterations were maximal on the 4 th day of unloading. The inhibitor of aSMase clomipramine attenuated ceramide accumulation, decreased pro-oxidant and pro-apoptotic activities and diminished muscle atrophy induced by unloading. It has been shown that in suspended for 14 days rats the loss in relative muscle mass, CSA and FD averaged -35%, -65% and -49%, respectively, whereas in clomipramine treated rats it was -25%, -45% and -25%, in comparison with the control values. Clomipramine also mitigated the inhibition of the mTORC1/p70S6 kinase inhibition caused by 14-day HS. Conclusions: The obtained results indicate the involvement of aSMase/ ceramide pathway in the development of disuse muscle atrophy. This effect may be triggered by TNFR1 and realized through enhanced prooxidant NADPH oxidase activity and pro-apoptotic signaling.

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Delphinidin prevents disuse muscle atrophy and reduces stress-related gene expression

Cited by 16 publications

References 25 publications

Allopurinol partially prevents disuse muscle atrophy in mice and humans

Allopurinol partially prevents disuse muscle atrophy in mice and humans

Flavonoids: nutraceutical potential for counteracting muscle atrophy

TNFa is Involved in the Development of Disuse Muscle Atrophy Through the Acid Sphingomyelinase/ Ceramide Up-Regulation and Pro-Oxidant Signaling

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