Resveratrol Ameliorates Palmitate-Induced Inflammation in Skeletal Muscle Cells by Attenuating Oxidative Stress and JNK/NF-κB Pathway in a SIRT1-Independent Mechanism

Sadeghi, Asie; Ebrahimi, Soltan Ahmad; Golestani, Abolfazl; Meshkani, Reza

doi:10.1002/jcb.25868

Cited by 76 publications

(50 citation statements)

References 52 publications

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“…As expected, the mitochondrial membrane potential and total ATP level were substantially reduced along with the reduction in the mitochondrial electron transport chain complex proteins in CCCP‐treated myotube cells (Figure A,B). Mitochondrial dysfunction is known to increase intracellular ROS generation . As shown in Figure C, the intracellular ROS levels were drastically elevated and the reduced by pretreatment with the antioxidant N‐acetylcysteine (NAC) in C2C12 myotubes.…”

Section: Resultsmentioning

confidence: 98%

“…Mitochondrial dysfunction is known to increase intracellular ROS generation. 22,23 As shown in Figure 3C, the intracellular ROS levels were drastically elevated and the reduced by pretreatment with the antioxidant N-acetylcysteine (NAC) in C2C12 myotubes. Next, we measured the proteins related to the mitochondrial dynamics and found that the levels of Mfn1, Mfn2 and the long form of OPA1 gradually decreased, while the expression of Fis1 increased upon treatment with CCCP and these effects were rescued by pretreatment with the antioxidant N-acetylcysteine (NAC) in C2C12 myotubes ( Figure 3D,E).…”

Section: Cccp-induced Mitochondrial Dysfunction Accompanies Muscle mentioning

confidence: 96%

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Down‐regulation of the mitochondrial i‐AAA protease Yme1L induces muscle atrophy via FoxO3a and myostatin activation

Lee

Kim

Park

et al. 2019

J Cellular Molecular Medi

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Muscle atrophy is closely associated with many diseases, including diabetes and cardiac failure. Growing evidence has shown that mitochondrial dysfunction is related to muscle atrophy; however, the underlying mechanisms are still unclear. To elucidate how mitochondrial dysfunction causes muscle atrophy, we used hindlimb‐immobilized mice. Mitochondrial function is optimized by balancing mitochondrial dynamics, and we observed that this balance shifted towards mitochondrial fission and that MuRF1 and atrogin‐1 expression levels were elevated in these mice. We also found that the expression of yeast mitochondrial escape 1‐like ATPase (Yme1L), a mitochondrial AAA protease was significantly reduced both in hindlimb‐immobilized mice and carbonyl cyanide m‐chlorophenylhydrazone (CCCP)‐treated C2C12 myotubes. When Yme1L was depleted in myotubes, the short form of optic atrophy 1 (Opa1) accumulated, leading to mitochondrial fragmentation. Moreover, a loss of Yme1L, but not of LonP1, activated AMPK and FoxO3a and concomitantly increased MuRF1 in C2C12 myotubes. Intriguingly, the expression of myostatin, a myokine responsible for muscle protein degradation, was significantly increased by the transient knock‐down of Yme1L. Taken together, our results suggest that a deficiency in Yme1L and the consequential imbalance in mitochondrial dynamics result in the activation of FoxO3a and myostatin, which contribute to the pathological state of muscle atrophy.

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Section: Resultsmentioning

confidence: 98%

Section: Cccp-induced Mitochondrial Dysfunction Accompanies Muscle mentioning

confidence: 96%

Down‐regulation of the mitochondrial i‐AAA protease Yme1L induces muscle atrophy via FoxO3a and myostatin activation

Lee

Kim

Park

et al. 2019

J Cellular Molecular Medi

View full text Add to dashboard Cite

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“…However, none of them are able to point out a compound as responsible for a specific action. Previous studies using other food sources or isolated bioactive compounds evidenced that phenolic compounds (for example, quercetin, chlorogenic acid, caffeic acid, and rosmarinic acid), dietary fiber, fatty acid (for example, ALA), and others play a role in repairing health conditions triggered by unbalanced diets (Gonzalez‐Manan et al., ; Pal & Ghosh, ; Sadeghi, Seyyed Ebrahimi, Golestani, & Meshkani, ). Nevertheless, regarding chia seed, it is hard to link the effect on metabolism to one specific compound.…”

Section: Resultsmentioning

confidence: 99%

Chia seed (Salvia hispanica L.) effects and their molecular mechanisms on unbalanced diet experimental studies: A systematic review

Enes

Moreira

Silva

et al. 2020

Journal of Food Science

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The aim of this review was to compile evidence and understand chia seed effects on unbalanced diet animal studies and the molecular mechanisms on metabolic biomarker modulation. A systematic review was conducted in electronic databases, following PRISMA recommendations. Risk of bias and quality was assessed using SYRCLE toll and ARRIVE guidelines. Seventeen articles were included. Throughout the studies, chia's main effects are associated with AMPK modulation: improvement of glucose and insulin tolerance, lipogenesis, antioxidant activity, and inflammation. Details about randomization and allocation concealment were insufficient, as well as information about blind protocols. Sample size, chia dose, and number of animals evaluated for each parameter were found to be lacking information among the studies. Based on experimental study data, chia has bioactive potential, and its daily consumption may reduce the risk of chronic disease development, mainly due to the antioxidant, anti-inflammatory, hypoglycemic, and hypolipidemic effects of the seed.Practical Application: The consumption of chia seeds may improve lipid profile, insulin and glucose tolerance, and reduce risk of cardiovascular disease. Whole seed or its oil presents positive effect, but the effects of chia oil can act faster than the seed.

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“…NF-κB was key to the inflammatory action due to its regulatory role on the expression of a variety of cytokines (such as TNF-α and IL-6) that regulate the inflammatory response (25,45). As a regulator of death and survival proteins, NF-κB serves an important role in neuron survival in the CNS.…”

Section: Discussionmentioning

confidence: 99%

Neuroprotective effect of combining tanshinone IIA with low-dose methylprednisolone following acute spinal cord injury in rats

Yao

Shi³

et al. 2017

Experimental and Therapeutic Medicine

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The present study compared the potential neuroprotective effect of tanshinone IIA (TIIA) monotherapy, methylprednisolone (MP) monotherapy and combined treatment in an adult acute spinal cord injury (ASCI) rat model. The current study used the weight-drop method (Allen's Impactor) in the rat model and the mechanical scratch method in primary spinal cord neuron culture to determine whether the combined treatment was able to reduce the required dosage of MP in the treatment of ASCI to produce a similar or improved therapeutic effect. In vivo male Sprague Dawley rats (n=60) were randomly divided into 5 groups, of which 12 rats were selected for the sham group and T9-T11 laminectomies, leading to ASCI, were performed on 48 of the 60 rats using a 10 g ×25 mm weight-drop at the level of T10 spinal cord. Therefore, the ASCI group (n=12) included the ‘laminectomy and weight-drop’. The remaining 36 ASCI model animals were subdivided into 3 groups (n=12 each group): TIIA group (30 mg/kg/day), MP group (30 mg/kg) and combined treatment group (TIIA 30 mg/kg/day + MP 20 mg/kg). Neuronal function following ASCI was evaluated using the Basso Beattie Bresnahan (BBB) locomotor rating scale. Levels of the anti-apoptotic factor B-cell lymphoma-2 (Bcl-2), the pro-apoptotic factors Bcl-2 associated protein X (Bax) and caspase-3, and the inflammatory associated factor nuclear factor-κB, were analyzed by western blot analysis. Immunohistochemistry was used to detect caspase-3. To investigate the underlying mechanism, the anti-oxidative effect of combination TIIA and MP treatment was assessed by measuring the activity of malondialdehyde (MDA) and superoxide dismutase (SOD) in ASCI. In agreement with the experiment in vivo, primary neurons were prepared from the spinal cord of one-day-old Sprague-Dawley rats' and co-cultured with astrocytes from the brain cortex. The injury of neurons was induced by mechanical scratch and levels of apoptosis factors were analyzed by western blot analysis. The results of the current study indicated that injured animals in the combined treatment group exhibited a significant increase in BBB scores (P<0.05). TIIA + MP combined treatment and MP treatment was observed to reduce the expression of pro-apoptotic factors and promote neuron survival in vivo and in vitro. Combined treatment may promote neuroprotection through reduced apoptosis and inflammation caused by ASCI, similar to MP alone. Combined treatment reversed the decrease of SOD and the increase of MDA level caused by ASCI. In addition, combined treatment decreased the expression of caspase-3 in the neurons following ASCI in rats, as indicated by immunofluorescence double labeling. Overall, the present study indicates that the combined treatment of TIIA and MP may protect the neurons by stimulating the rapid initiation of neuroprotection following ASCI and reduce the dosage of MP in the treatment of ASCI required to produce the same or improved neuroprotective effects in vivo and in vitro.

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Resveratrol Ameliorates Palmitate-Induced Inflammation in Skeletal Muscle Cells by Attenuating Oxidative Stress and JNK/NF-κB Pathway in a SIRT1-Independent Mechanism

Cited by 76 publications

References 52 publications

Down‐regulation of the mitochondrial i‐AAA protease Yme1L induces muscle atrophy via FoxO3a and myostatin activation

Down‐regulation of the mitochondrial i‐AAA protease Yme1L induces muscle atrophy via FoxO3a and myostatin activation

Chia seed (Salvia hispanica L.) effects and their molecular mechanisms on unbalanced diet experimental studies: A systematic review

Neuroprotective effect of combining tanshinone IIA with low-dose methylprednisolone following acute spinal cord injury in rats

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