scholarly journals Curcumin and Resveratrol Improve Muscle Function and Structure through Attenuation of Proteolytic Markers in Experimental Cancer-Induced Cachexia

Molecules ◽  
2021 ◽  
Vol 26 (16) ◽  
pp. 4904
Author(s):  
Antonio Penedo-Vázquez ◽  
Xavier Duran ◽  
Javier Mateu ◽  
Adrián López-Postigo ◽  
Esther Barreiro
Keyword(s):  
Signaling Pathways ◽  
Muscle Wasting ◽  
Troponin I ◽  
Total Body Weight ◽  
Sirtuin 1 ◽  
Limb Muscle ◽  
Cross Sectional ◽  
Therapeutic Implications ◽  
Beneficial Effects ◽  
Muscle Mass Loss

Muscle wasting and cachexia are prominent comorbidities in cancer. Treatment with polyphenolic compounds may partly revert muscle wasting. We hypothesized that treatment with curcumin or resveratrol in cancer cachectic mice may improve muscle phenotype and total body weight through attenuation of several proteolytic and signaling mechanisms in limb muscles. In gastrocnemius and soleus muscles of cancer cachectic mice (LP07 adenocarcinoma cells, N = 10/group): (1) LC-induced cachexia, (2) LC-cachexia+curcumin, and (3) LC-cachexia + resveratrol, muscle structure and damage (including blood troponin I), sirtuin-1, proteolytic markers, and signaling pathways (NF-κB and FoxO3) were explored (immunohistochemistry and immunoblotting). Compared to nontreated cachectic mice, in LC-cachexia + curcumin and LC-cachexia + resveratrol groups, body and muscle weights (gastrocnemius), limb muscle strength, muscle damage, and myofiber cross-sectional area improved, and in both muscles, sirtuin-1 increased, while proteolysis (troponin I), proteolytic markers, and signaling pathways were attenuated. Curcumin and resveratrol elicited beneficial effects on fast- and slow-twitch limb muscle phenotypes in cachectic mice through sirtuin-1 activation, attenuation of atrophy signaling pathways, and proteolysis in cancer cachectic mice. These findings have future therapeutic implications as these natural compounds, separately or in combination, may be used in clinical settings of muscle mass loss and dysfunction including cancer cachexia.

scholarly journals Beneficial Effects of Resveratrol in Mouse Gastrocnemius: A Hint to Muscle Phenotype and Proteolysis

Cells ◽  
2021 ◽  
Vol 10 (9) ◽  
pp. 2436
Author(s):  
Laura Mañas-García ◽  
Charlotte Denhard ◽  
Javier Mateu ◽  
Xavier Duran ◽  
Joaquim Gea ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Muscle Fiber ◽  
Troponin I ◽  
Muscle Protein ◽  
Strength Loss ◽  
Muscle Weight ◽  
Cross Sectional ◽  
Therapeutic Implications ◽  
Resveratrol Treatment ◽  
And Function

We hypothesized that the phenolic compound resveratrol mitigates muscle protein degradation and loss and improves muscle fiber cross-sectional area (CSA) in gastrocnemius of mice exposed to unloading (7dI). In gastrocnemius of mice (female C57BL/6J, 10 weeks) exposed to a seven-day period of hindlimb immobilization with/without resveratrol treatment, markers of muscle proteolysis (tyrosine release, systemic troponin-I), atrophy signaling pathways, and muscle phenotypic features and function were analyzed. In gastrocnemius of unloaded mice treated with resveratrol, body and muscle weight and function were attenuated, whereas muscle proteolysis (tyrosine release), proteolytic and apoptotic markers, atrophy signaling pathways, and myofiber CSA significantly improved. Resveratrol treatment of mice exposed to a seven-day period of unloading prevented body and muscle weight and limb strength loss, while an improvement in muscle proteolysis, proteolytic markers, atrophy signaling pathways, apoptosis, and muscle fiber CSA was observed in the gastrocnemius muscle. These findings may have potential therapeutic implications in the management of disuse muscle atrophy in clinical settings.

scholarly journals Troponin I Changes in Patients with Subarachnoid Hemorrhage

2018 ◽  
Vol 27 (2) ◽  
pp. 39-43
Author(s):  
A Sarker ◽  
MA Hoque ◽  
MMR Khan ◽  
MK Rahman ◽  
SM Alam ◽  
...  
Keyword(s):  
Subarachnoid Hemorrhage ◽  
Troponin I ◽  
Cardiac Injury ◽  
Neurological Injury ◽  
Enzyme Release ◽  
College Hospital ◽  
Cross Sectional ◽  
Therapeutic Implications ◽  
Patients At Risk ◽  
Ctni Level

Background : Subarachnoid hemorrhage (SAH) is a catastrophic neurological event. Aside from its neurological morbidities, SAH is associated with significant medical complications. Cardiac manifestations are common and can impact morbidity and mortality in SAH patients. Myocardial enzyme release occur frequently after Subarachnoid hemorrhage that reflect adverse intracranial events .These changes often are unrecognized or misinterpreted, potentially placing patients at risk for inappropriate management.Objective : The aim of this study was to assess Troponin I changes after acute SAH and these changes were compared with neurological severity. The result of the study might be helpful for better understanding diagnostic and therapeutic implications of acute neurocardiogenic injury after SAH.Patients and methods : This cross sectional descriptive study was conducted over 30 patients with SAH in medicine, neuromedicine and intensive care unit of Rajshahi Medical College Hospital during the period of January 2015 to December 2016. Predictor variables reflecting demographic (age, sex, occupation), hemodynamic (pulse, systolic and diastolic blood pressure) and neurological (WFNS score) informations were recorded. We evaluated their cTnI level, which had been measured at admission. A cTnI level above 0.12 ng/ml was defined as an indicator of cardiac injury following SAH.Results : Out of 30 patients 26.7% were both in between 40-49 years and 60-69 years age group & 50% were male and 50% were female. Among the risk factors 60% of patient had history of hypertension, 40% smoking, 10% Diabetes mellitus and 3.3% alcohol abuse. On admission the mean GCS was 12.53±2.69,. The most frequently occurring WFNS grading were grade 1 and grade 4 (both were 43.3% of patients). Out of Thirty, 43.3% of patients demonstrated elevations of Troponin I. WFNS score ≥ 3 (92.3%, p = <0.001) significantly correlated with elevated Troponin I concentration.Conclusion : serum troponin I reveal a higher incidence of myocardial injury in patients with SAH. The present study also demonstrates that raised serum cTnI is associated with more severe neurological injury. These findings support a neurocardiogenic cause of cardiac injury after SAH.TAJ 2014; 27(2): 39-43

scholarly journals Muscle Phenotype, Proteolysis, and Atrophy Signaling During Reloading in Mice: Effects of Curcumin on the Gastrocnemius

Nutrients ◽  
2020 ◽  
Vol 12 (2) ◽  
pp. 388 ◽  
Author(s):  
Laura Mañas-García ◽  
Nuria Bargalló ◽  
Joaquim Gea ◽  
Esther Barreiro
Keyword(s):  
Protein Synthesis ◽  
Signaling Pathways ◽  
Muscle Function ◽  
Histone Deacetylases ◽  
Troponin I ◽  
Muscle Protein ◽  
Sirtuin 1 ◽  
Hybrid Fibers ◽  
Disuse Muscle Atrophy ◽  
And Function

We hypothesized that curcumin may mitigate muscle protein degradation and loss through attenuation of proteolytic activity in limb muscles of mice exposed to reloading (7dR) following immobilization (7dI). In gastrocnemius of mice (female C57BL/6J, 10 weeks) exposed to recovery following a seven-day period of hindlimb immobilization with/without curcumin treatment, markers of muscle proteolysis (systemic troponin-I), atrophy signaling pathways and histone deacetylases, protein synthesis, and muscle phenotypic characteristics and function were analyzed. In gastrocnemius of reloading mice compared to unloaded, muscle function, structure, sirtuin-1, and protein synthesis improved, while proteolytic and signaling markers (FoxO1/3) declined. In gastrocnemius of unloaded and reloaded mice treated with curcumin, proteolytic and signaling markers (NF-kB p50) decreased and sirtuin-1 activity and hybrid fibers size increased (reloaded muscle), while no significant improvement was seen in muscle function. Treatment with curcumin elicited a rise in sirtuin-1 activity, while attenuating proteolysis in gastrocnemius of mice during reloading following a period of unloading. Curcumin attenuated muscle proteolysis probably via activation of histone deacetylase sirtuin-1, which also led to decreased levels of atrophy signaling pathways. These findings offer an avenue of research in the design of therapeutic strategies in clinical settings of patients exposed to periods of disuse muscle atrophy.

scholarly journals Prolonged Immobilization Exacerbates the Loss of Muscle Mass and Function Induced by Cancer-Associated Cachexia through Enhanced Proteolysis in Mice

2020 ◽  
Vol 21 (21) ◽  
pp. 8167
Author(s):  
Laura Mañas-García ◽  
Antonio Penedo-Vázquez ◽  
Adrián López-Postigo ◽  
Jorieke Deschrevel ◽  
Xavier Durán ◽  
...  
Keyword(s):  
Muscle Damage ◽  
Muscle Mass ◽  
Muscle Regeneration ◽  
Troponin I ◽  
Hindlimb Unloading ◽  
Cross Sectional ◽  
Muscle Mass Loss ◽  
Prolonged Immobilization ◽  
And Function ◽  
Fast Twitch

We hypothesized that in mice with lung cancer (LC)-induced cachexia, periods of immobilization of the hindlimb (7 and 15 days) may further aggravate the process of muscle mass loss and function. Mice were divided into seven groups (n = 10/group): (1) non-immobilized control mice, (2) 7-day unloaded mice (7-day I), (3) 15-day unloaded mice (15-day I), (4) 21-day LC-cachexia group (LC 21-days), (5) 30-day LC-cachexia group (LC 30-days), (6) 21-day LC-cachexia group besides 7 days of unloading (LC 21-days + 7-day I), (7) 30-day LC-cachexia group besides 15 days of unloading (LC 30-days + 15-day I). Physiological parameters, body weight, muscle and tumor weights, phenotype and morphometry, muscle damage (including troponin I), proteolytic and autophagy markers, and muscle regeneration markers were identified in gastrocnemius muscle. In LC-induced cachexia mice exposed to hindlimb unloading, gastrocnemius weight, limb strength, fast-twitch myofiber cross-sectional area, and muscle regeneration markers significantly decreased, while tumor weight and area, muscle damage (troponin), and proteolytic and autophagy markers increased. In gastrocnemius of cancer-cachectic mice exposed to unloading, severe muscle atrophy and impaired function was observed along with increased muscle proteolysis and autophagy, muscle damage, and impaired muscle regeneration.

Association of Vitamin D Status With Liver and Kidney Disease: A Systematic Review of Clinical Trials, and Cross-Sectional and Cohort Studies

2019 ◽  
pp. 1-13 ◽  
Author(s):  
Seyed Mostafa Parizadeh ◽  
Majid Rezayi ◽  
Reza Jafarzadeh-Esfehani ◽  
Amir Avan ◽  
Hamideh Ghazizadeh ◽  
...  
Keyword(s):  
Vitamin D ◽  
Kidney Disease ◽  
Renal Disease ◽  
Cohort Studies ◽  
Cochrane Library ◽  
Major Public Health Problem ◽  
Vitamin D Status ◽  
Cross Sectional ◽  
Beneficial Effects ◽  
Vitamin D Levels

Abstract. Background: Vitamin D deficiency (VDD) is a major public health problem. There are few comprehensive systematic reviews about the relationship between Vitamin D status and liver and renal disease in Iran. Methods: We systemically searched the following databases: Web of Science; PubMed; Cochrane Library; Scopus; Science Direct; Google Scholar and two Iranian databases (Scientific Information Database (SID) and IranMedex) up until November 2017 to identify all randomized control trials (RCTs), case control, cross-sectional and cohort studies investigating the association between vitamin D and any form of liver or kidney disease. Results: Vitamin D insufficiency, or deficiency (VDD), is highly prevalent in Iran, reports varying between 44.4% in Isfahan to 98% in Gorgan. There is also a high prevalence of VDD among patients with liver or kidney disease, and the administration of vitamin D supplements may have beneficial effects on lipid profile, blood glucose, liver function and fatty liver disease, and bone health. Low serum vitamin D levels are related with abnormalities in these laboratory and clinical parameters. Conclusion: VDD is prevalent in patients with chronic liver or renal disease in Iran. There appear to be several beneficial effects of vitamin D supplementation in vitamin D deficient patients with liver or kidney disease.

scholarly journals Curcumin: Modulator of Key Molecular Signaling Pathways in Hormone-Independent Breast Cancer

Cancers ◽  
2021 ◽  
Vol 13 (14) ◽  
pp. 3427
Author(s):  
Reyhaneh Farghadani ◽  
Rakesh Naidu
Keyword(s):  
Breast Cancer ◽  
Signaling Pathways ◽  
Mapk Pathway ◽  
Growth Factor Receptor ◽  
Progesterone Receptors ◽  
Drug Candidate ◽  
Molecular Signaling ◽  
Her2 Positive ◽  
Therapeutic Implications ◽  
Epidermal Growth

Breast cancer is the most frequently diagnosed cancer and the leading cause of cancer death among women worldwide. Despite the overall successes in breast cancer therapy, hormone-independent HER2 negative breast cancer, also known as triple negative breast cancer (TNBC), lacking estrogens and progesterone receptors and with an excessive expression of human epidermal growth factor receptor 2 (HER2), along with the hormone-independent HER2 positive subtype, still remain major challenges in breast cancer treatment. Due to their poor prognoses, aggressive phenotype, and highly metastasis features, new alternative therapies have become an urgent clinical need. One of the most noteworthy phytochemicals, curcumin, has attracted enormous attention as a promising drug candidate in breast cancer prevention and treatment due to its multi-targeting effect. Curcumin interrupts major stages of tumorigenesis including cell proliferation, survival, angiogenesis, and metastasis in hormone-independent breast cancer through the modulation of multiple signaling pathways. The current review has highlighted the anticancer activity of curcumin in hormone-independent breast cancer via focusing on its impact on key signaling pathways including the PI3K/Akt/mTOR pathway, JAK/STAT pathway, MAPK pathway, NF-ĸB pathway, p53 pathway, and Wnt/β-catenin, as well as apoptotic and cell cycle pathways. Besides, its therapeutic implications in clinical trials are here presented.

Molecular mechanisms of doxorubicin-induced cardiotoxicity: novel roles of sirtuin 1-mediated signaling pathways

2021 ◽  
Author(s):  
Jie Wang(a) ◽  
Jingjing Zhang ◽  
Mengjie Xiao ◽  
Shudong Wang ◽  
Jie Wang(b) ◽  
...  
Keyword(s):  
Signaling Pathways ◽  
Molecular Mechanisms ◽  
Sirtuin 1

scholarly journals Cytokine signaling convergence regulates the microglial state transition in Alzheimer’s disease

2021 ◽  
Author(s):  
Shun-Fat Lau ◽  
Amy K. Y. Fu ◽  
Nancy Y. Ip
Keyword(s):  
Alzheimer’S Disease ◽  
Alzheimer's Disease ◽  
Signaling Pathways ◽  
State Transition ◽  
Cytokine Signaling ◽  
Interleukin 33 ◽  
Beneficial Effects ◽  
Activated State ◽  
Therapeutic Development ◽  
Functional States

AbstractGenetic analyses have revealed the pivotal contribution of microglial dysfunctions to the pathogenesis of Alzheimer’s disease (AD). Along AD progression, the accumulation of danger-associated molecular patterns (DAMPs) including beta-amyloid and hyperphosphorylated tau continuously stimulates microglia, which results in their chronic activation. Chronically activated microglia secrete excessive pro-inflammatory cytokines, which further regulate microglial responses towards DAMPs. This has spurred longstanding interest in targeting cytokine-induced microglial responses for AD therapeutic development. However, the cytokine-induced microglial state transition is not comprehensively understood. Cytokines are assumed to induce microglial state transition from a resting state to an activated state. However, recent evidence indicate that this microglial state transition involves multiple sequential functional states. Moreover, the mechanisms by which different functional states within the cytokine-induced microglial state transition regulate AD pathology remain unclear. In this review, we summarize how different cytokine signaling pathways, including those of IL-33 (interleukin-33), NLRP3 inflammasome–IL-1β, IL-10, and IL-12/IL-23, regulate microglial functions in AD. Furthermore, we discuss how the modulation of these cytokine signaling pathways can result in beneficial outcomes in AD. Finally, we describe a stepwise functional state transition of microglia induced by cytokine signaling that can provide insights into the molecular basis of the beneficial effects of cytokine modulation in AD and potentially aid therapeutic development.

Decline of contractility during ischemia-reperfusion injury: actin glutathionylation and its effect on allosteric interaction with tropomyosin

2006 ◽  
Vol 290 (3) ◽  
pp. C719-C727 ◽  
Author(s):  
Frank C. Chen ◽  
Ozgur Ogut
Keyword(s):  
Reperfusion Injury ◽  
Posttranslational Modifications ◽  
Actin Polymerization ◽  
Time Course ◽  
Troponin I ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
High Concentration ◽  
Cross Sectional ◽  
The Impact

The severity and duration of ischemia-reperfusion injury is hypothesized to play an important role in the ability of the heart subsequently to recover contractility. Permeabilized trabeculae were prepared from a rat model of ischemia-reperfusion injury to examine the impact on force generation. Compared with the control perfused condition, the maximum force (Fmax) per cross-sectional area and the rate of tension redevelopment of Ca2+-activated trabeculae fell by 71% and 44%, respectively, during ischemia despite the availability of a high concentration of ATP. The reduction in Fmax with ischemia was accompanied by a decline in fiber stiffness, implying a drop in the absolute number of attached cross bridges. However, the declines during ischemia were largely recovered after reperfusion, leading to the hypothesis that intrinsic, reversible posttranslational modifications to proteins of the contractile filaments occur during ischemia-reperfusion injury. Examination of thin-filament proteins from ischemic or ischemia-reperfused hearts did not reveal proteolysis of troponin I or T. However, actin was found to be glutathionylated with ischemia. Light-scattering experiments demonstrated that glutathionylated G-actin did not polymerize as efficiently as native G-actin. Although tropomyosin accelerated the time course of native and glutathionylated G-actin polymerization, the polymerization of glutathionylated G-actin still lagged native G-actin at all concentrations of tropomyosin tested. Furthermore, cosedimentation experiments demonstrated that tropomyosin bound glutathionylated F-actin with significantly reduced cooperativity. Therefore, glutathionylated actin may be a novel contributor to the diverse set of posttranslational modifications that define the function of the contractile filaments during ischemia-reperfusion injury.

scholarly journals Plant Foods Rich in Antioxidants and Human Cognition: A Systematic Review

Antioxidants ◽  
2021 ◽  
Vol 10 (5) ◽  
pp. 714
Author(s):  
Luciana Baroni ◽  
Anna Rita Sarni ◽  
Cristina Zuliani
Keyword(s):  
Young Adult ◽  
Human Cognition ◽  
Cognitive Assessments ◽  
Cross Sectional ◽  
Cognitive Domains ◽  
Plant Foods ◽  
Beneficial Effects ◽  
System Integrity ◽  
Plant Antioxidants ◽  
The Impact

Oxidative stress can compromise central nervous system integrity, thereby affecting cognitive ability. Consumption of plant foods rich in antioxidants could thereby protect cognition. We systematically reviewed the literature exploring the effects of antioxidant-rich plant foods on cognition. Thirty-one studies were included: 21 intervention, 4 cross-sectional (one with a cohort in prospective observation as well), and 6 prospective studies. Subjects belonged to various age classes (young, adult, and elderly). Some subjects examined were healthy, some had mild cognitive impairment (MCI), and some others were demented. Despite the different plant foods and the cognitive assessments used, the results can be summarized as follows: 7 studies reported a significant improvement in all cognitive domains examined; 19 found significant improvements only in some cognitive areas, or only for some food subsets; and 5 showed no significant improvement or no effectiveness. The impact of dietary plant antioxidants on cognition appears promising: most of the examined studies showed associations with significant beneficial effects on cognitive functions—in some cases global or only in some specific domains. There was typically an acute, preventive, or therapeutic effect in young, adult, and elderly people, whether they were healthy, demented, or affected by MCI. Their effects, however, are not attributable only to anti-oxidation.

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