scholarly journals Polyphenols as Therapeutic Approach to High Altitude Mediated Skeletal Muscle Impairments

2021 ◽  
Vol 6 (4) ◽  
pp. 314-322
Author(s):  
Asha Devi Kushwaha ◽  
Varun Bhardwaj ◽  
Deepika Saraswat
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Review Article ◽  
Physical Activities ◽  
Skeletal Muscle Atrophy ◽  
Therapeutic Effects ◽  
Natural Polyphenols ◽  
Pathological Conditions ◽  
Anti Inflammatory

Skeletal muscle impairments at high altitudes resulted into various consequences in un-acclimatised individuals thus hampering their physical activities by imposing severe oxidative stress, skeletal muscle atrophy, mitochondrial dysfunction/autophagy, and regeneration disability. Researchers have described many natural and synthetic supplements to alleviate oxidative stress-induced muscle impairments. In this review article we are focusing on the skeletal muscle impairments and their alleviation by using natural polyphenols. Polyphenols are plant-based compounds showing anti-oxidative and anti-inflammatory properties like Curcumin, Catechins, Resveratrol, Quercetin and Salidrosides appear to mainly act by reversing oxidative stress and mitochondrial dysfunction eventually ameliorate skeletal muscle impairments under various imposed pathological conditions. This review also drew attention on the molecular targets of polyphenols and their possible therapeutic effects in preventing HA induced muscle impairments. Unavailability of suitable intervention, there is a need to find a probable solution having highly protective anti-atrophic, anti-oxidative, anti-inflammatory properties with the tint of performance enhancer.

scholarly journals Role of Oxidative Stress as Key Regulator of Muscle Wasting during Cachexia

2018 ◽  
Vol 2018 ◽  
pp. 1-17 ◽  
Author(s):  
Johanna Ábrigo ◽  
Alvaro A. Elorza ◽  
Claudia A. Riedel ◽  
Cristian Vilos ◽  
Felipe Simon ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Protein Synthesis ◽  
Mitochondrial Dysfunction ◽  
Protein Modification ◽  
Molecular Mechanisms ◽  
Pathological Condition ◽  
Stress Protein ◽  
Skeletal Muscle Atrophy ◽  
Regulate Protein

Skeletal muscle atrophy is a pathological condition mainly characterized by a loss of muscular mass and the contractile capacity of the skeletal muscle as a consequence of muscular weakness and decreased force generation. Cachexia is defined as a pathological condition secondary to illness characterized by the progressive loss of muscle mass with or without loss of fat mass and with concomitant diminution of muscle strength. The molecular mechanisms involved in cachexia include oxidative stress, protein synthesis/degradation imbalance, autophagy deregulation, increased myonuclear apoptosis, and mitochondrial dysfunction. Oxidative stress is one of the most common mechanisms of cachexia caused by different factors. It results in increased ROS levels, increased oxidation-dependent protein modification, and decreased antioxidant system functions. In this review, we will describe the importance of oxidative stress in skeletal muscles, its sources, and how it can regulate protein synthesis/degradation imbalance, autophagy deregulation, increased myonuclear apoptosis, and mitochondrial dysfunction involved in cachexia.

Role of Oxidative Stress and Mitochondrial Dysfunction in Skeletal Muscle in Type 2 Diabetic Patients

2016 ◽  
Vol 22 (18) ◽  
pp. 2650-2656 ◽  
Author(s):  
Noelia Diaz-Morales ◽  
Susana Rovira-Llopis ◽  
Irene Escribano-Lopez ◽  
Celia Bañuls ◽  
Sandra Lopez-Domenech ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Mitochondrial Dysfunction ◽  
Diabetic Patients ◽  
Type 2 Diabetic Patients ◽  
Type 2 Diabetic

scholarly journals Hydrogen sulfide alleviates hyperhomocysteinemia-mediated skeletal muscle atrophy via mitigation of oxidative and endoplasmic reticulum stress injury

2018 ◽  
Vol 315 (5) ◽  
pp. C609-C622 ◽  
Author(s):  
Avisek Majumder ◽  
Mahavir Singh ◽  
Jyotirmaya Behera ◽  
Nicholas T. Theilen ◽  
Akash K. George ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Skeletal Muscle ◽  
Endoplasmic Reticulum ◽  
Hydrogen Sulfide ◽  
Er Stress ◽  
Muscle Atrophy ◽  
C2c12 Cells ◽  
Skeletal Muscle Atrophy ◽  
Stress Injury ◽  
Western Blots

Although hyperhomocysteinemia (HHcy) occurs because of the deficiency in cystathionine-β-synthase (CBS) causing skeletal muscle dysfunction, it is still unclear whether this effect is mediated through oxidative stress, endoplasmic reticulum (ER) stress, or both. Nevertheless, there is no treatment option available to improve HHcy-mediated muscle injury. Hydrogen sulfide (H2S) is an antioxidant compound, and patients with CBS mutation do not produce H2S. In this study, we hypothesized that H2S mitigates HHcy-induced redox imbalance/ER stress during skeletal muscle atrophy via JNK phosphorylation. We used CBS+/−mice to study HHcy-mediated muscle atrophy, and treated them with sodium hydrogen sulfide (NaHS; an H2S donor). Proteins and mRNAs were examined by Western blots and quantitative PCR. Proinflammatory cytokines were also measured. Muscle mass and strength were studied via fatigue susceptibility test. Our data revealed that HHcy was detrimental to skeletal mass, particularly gastrocnemius and quadriceps muscle weight. We noticed that oxidative stress was reversed by NaHS in homocysteine (Hcy)-treated C2C12 cells. Interestingly, ER stress markers (GRP78, ATF6, pIRE1α, and pJNK) were elevated in vivo and in vitro, and NaHS mitigated these effects. Additionally, we observed that JNK phosphorylation was upregulated in C2C12 after Hcy treatment, but NaHS could not reduce this effect. Furthermore, inflammatory cytokines IL-6 and TNF-α were higher in plasma from CBS as compared with wild-type mice. FOXO1-mediated Atrogin-1 and MuRF-1 upregulation were attenuated by NaHS. Functional studies revealed that NaHS administration improved muscle fatigability in CBS+/−mice. In conclusion, our work provides evidence that NaHS is beneficial in mitigating HHcy-mediated skeletal injury incited by oxidative/ER stress responses.

Abstract 16009: Y RNA Fragments Enriched in Exosomes From Cardiosphere-derived Cells Mediate Cardioprotection and Macrophage Polarization

Circulation ◽  
2015 ◽  
Vol 132 (suppl_3) ◽  
Author(s):  
Linda Cambier ◽  
Geoffrey de Couto ◽  
Ahmed Ibrahim ◽  
Eduardo Marbán
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Noncoding Rna ◽  
Neonatal Rat ◽  
Target Cells ◽  
Therapeutic Effects ◽  
Data Set ◽  
Rna Content ◽  
Rna Fragments ◽  
Anti Inflammatory

Background: Exosomes secreted by cardiosphere-derived cells (CDCs) are critical agents of regeneration and cardioprotection following ischemic injury, mediating the beneficial therapeutic effects of CDCs. Transfer of exosomal RNA to target cells is important for bioactivity. Objective: We sought to determine the RNA content of CDCs-secreted exosomes (CDC-exo), and to assess the contributions of selected small non-coding RNAs to the therapeutic efficacy of CDC-exo. Methods: Using next-generation sequencing (Illumina), we characterized the RNA content of CDC-exo. By direct transfection of fluorescently-labelled oligoribonucleotides, we delivered and tracked selected RNA fragments that are highly enriched in CDC-exo. In order to examine potential cytoprotective effects, neonatal rat ventricular myocytes (NRVMs) were pretreated with each of these fragments or a scrambled control fragment prior to H2O2-induced oxidative stress. Effects on gene expression were assessed by transfection of the fragments into bone marrow-derived macrophages. Results: Several noncoding RNA species were present in CDC-exo. Among these, Y RNAs (either whole or in fragments of the 5’ end) constituted 18% of all hits. From this data set, we selected two highly-enriched Y RNA fragments. Both fragments localized to the cytoplasm of CDC, NRVM and macrophages, and conferred augmented resistance to oxidative stress of NRVM (64.25±31.13% viability vs. 44±26.85%; p=0.06). Additionally, macrophages transfected with Y fragments exhibit rapid, robust polarization to a distinctive gene expression profile notable for upregulation of IL-10 (83.07 vs. 0.59 fold; p<0.0001), an anti-inflammatory cytokine. Conclusions: Here, we demonstrated that abundant noncoding RNA components of CDC-exo, Y RNA fragments, are bioactive components of CDC-exo. Two distinct fragments confer cardioprotection and also induce a strong anti-inflammatory response in macrophages. Although several components of the CDC-exo payload (including miRNA) contribute to functional efficacy, the present findings demonstrate the capacity of Y RNA fragments, an RNA species of previously-unknown function, to elicit therapeutic effects in vitro.

scholarly journals Mitochondrial donation in translational medicine; from imagination to reality

2020 ◽  
Vol 18 (1) ◽  
Author(s):  
Hesam Saghaei Bagheri ◽  
Farhad Bani ◽  
Savas Tasoglu ◽  
Amir Zarebkohan ◽  
Reza Rahbarghazi ◽  
...  
Keyword(s):  
Translational Medicine ◽  
Specific Activity ◽  
Current Knowledge ◽  
Review Article ◽  
Target Cells ◽  
Therapeutic Effects ◽  
Cellular Mechanisms ◽  
Pathological Conditions ◽  
Mitochondrial Transfer ◽  
Mitochondrial Donation

Abstract The existence of active crosstalk between cells in a paracrine and juxtacrine manner dictates specific activity under physiological and pathological conditions. Upon juxtacrine interaction between the cells, various types of signaling molecules and organelles are regularly transmitted in response to changes in the microenvironment. To date, it has been well-established that numerous parallel cellular mechanisms participate in the mitochondrial transfer to modulate metabolic needs in the target cells. Since the conception of stem cells activity in the restoration of tissues’ function, it has been elucidated that these cells possess a unique capacity to deliver the mitochondrial package to the juxtaposed cells. The existence of mitochondrial donation potentiates the capacity of modulation in the distinct cells to achieve better therapeutic effects. This review article aims to scrutinize the current knowledge regarding the stem cell’s mitochondrial transfer capacity and their regenerative potential.

scholarly journals Exercise as an anti-inflammatory therapy for cancer cachexia: a focus on interleukin-6 regulation

2020 ◽  
Vol 318 (2) ◽  
pp. R296-R310 ◽  
Author(s):  
Hélène N. Daou
Keyword(s):  
Skeletal Muscle ◽  
Systemic Inflammation ◽  
Cancer Cachexia ◽  
Muscle Wasting ◽  
Skeletal Muscle Atrophy ◽  
Ampk Signaling ◽  
Skeletal Muscle Wasting ◽  
Skeletal Muscle Loss ◽  
Anti Inflammatory ◽  
Tumor Growth And Metastasis

Cancer cachexia is a complicated disorder of extreme, progressive skeletal muscle wasting. It is directed by metabolic alterations and systemic inflammation dysregulation. Numerous studies have demonstrated that increased systemic inflammation promotes this type of cachexia and have suggested that cytokines are implicated in the skeletal muscle loss. Exercise is firmly established as an anti-inflammatory therapy that can attenuate or even reverse the process of muscle wasting in cancer cachexia. The interleukin IL-6 is generally considered to be a key player in the development of the microenvironment of malignancy; it promotes tumor growth and metastasis by acting as a bridge between chronic inflammation and cancerous tissue and it also induces skeletal muscle atrophy and protein breakdown. Paradoxically, a beneficial role for IL-6 has also been identified recently, and that is its status as a “founding member” of the myokine class of proteins. Skeletal muscle is an important source of circulating IL-6 in people who participate in exercise training. IL-6 acts as an anti-inflammatory myokine by inhibiting TNFα and improving glucose uptake through the stimulation of AMPK signaling. This review discusses the action of IL-6 in skeletal muscle tissue dysfunction and the role of IL-6 as an “exercise factor” that modulates the immune system. This review also sheds light on the main considerations related to the treatment of muscle wasting in cancer cachexia.

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