astaxanthine and Muscular-Atrophy

Cachexia, which is often marked by skeletal muscular atrophy, is one of the leading causes of death in cancer patients. Astaxanthin, a carotenoid obtained from marine organisms that can aid in the prevention and treatment of a variety of disorders. In this study, to assess whether astaxanthin ameliorates weight loss and skeletal muscle atrophy in sorafenib-treated hepatocellular carcinoma mice is aimed.. The findings show the significant potential of astaxanthin as nutritional supplements for cancer patients, as well as the notion that nutritional interventions should be implemented at the initiation of cancer treatment, as instead of waiting until cachexia sets in.

Topics: Animals; Cachexia; Dietary Supplements; Glucose; Mice; Muscle, Skeletal; Muscular Atrophy; Phosphatidylinositol 3-Kinases; Sorafenib; Weight Loss

Astaxanthin (AX) is a carotenoid that exerts potent antioxidant activity and acts in the lipid bilayer. This study aimed to investigate the effects of AX on muscle-atrophy-mediated disturbance of mitochondria, which have a lipid bilayer. Tail suspension was used to establish a muscle-atrophied mouse model. AX diet fed to tail-suspension mice prevented loss of muscle weight, inhibited the decrease of myofiber size, and restrained the increase of hydrogen peroxide (H

Topics: Animals; Antioxidants; Apoptosis; Caspase 3; Disease Models, Animal; Down-Regulation; Hindlimb Suspension; Hydrogen Peroxide; Male; Mice; Mice, Inbred C57BL; Mitochondria; Muscle Fibers, Skeletal; Muscle, Skeletal; Muscular Atrophy; Oxidative Stress; PPAR gamma; Reactive Oxygen Species; Up-Regulation; Xanthophylls

The antioxidant factors, astaxanthin, β-carotene, and resveratrol, have a potential effect on protein synthesis in skeletal muscle and a combined intake may have a greater cumulative effect than individual intake. The aim of this study was to investigate the combined effects on skeletal muscle mass and protein metabolic signaling during the hypertrophic process from atrophy in mice.. Male ICR mice were divided into five dietary groups consisting of seven animals each: normal, astaxanthin, β-carotene, resveratrol, and all three antioxidants. Equal concentrations (0.06% [w/w]) of the respective antioxidants were included in the diet of each group. In the mixed group, three antioxidants were added in equal proportion. One leg of each mouse was casted for 3 wk to induce muscle atrophy. After removal of the cast, the mice were fed each diet for 2 wk. The muscle tissues were collected, weighed, and examined for protein metabolism signaling and oxidative damage.. The weight of the soleus muscle was increased in the astaxanthin, β-carotene, and resveratrol groups to a greater extent than in the normal group; this was accelerated by intake of the mixed antioxidants (P = 0.007). Phosphorylation levels of mammalian target of rapamycin and p70 S6 K in the muscle were higher in the mixed antioxidant group than in the normal group (P = 0.025; P = 0.020). The carbonylated protein concentration was lower in the mixed antioxidant group than in the normal group (P = 0.021).. These results suggested that a combination of astaxanthin, β-carotene, and resveratrol, even in small amounts, promoted protein synthesis during the muscle hypertrophic process following atrophy.

Topics: Animals; Antioxidants; beta Carotene; Diet; Hypertrophy; Male; Mice; Mice, Inbred ICR; Muscle, Skeletal; Muscular Atrophy; Oxidative Stress; Protein Biosynthesis; Resveratrol; Xanthophylls

The effects of a combination of the antioxidant astaxanthin (AX) and electrical stimulation (ES) on muscle mass and mitochondrial oxidative capacity were investigated in the soleus muscle of hindlimb unloaded rats. Five groups of male Sprague-Dawley rats were used; control, 1-week hindlimb unloading (HU), HU + AX, HU + ES, and HU + AX + ES. Respective rats in the AX groups received 50-mg/kg AX twice daily during HU. Calf muscles of rats in the ES groups were electrically stimulated for 240 s/day during HU. One-week HU decreased muscle mass along with decreased FoxO3a phosphorylation and increased ubiquitinated proteins expressions, decreased oxidative enzymatic activity accompanied with decline in PGC-1α protein expression, and increased reactive oxygen species production. However, the combination treatment could synergistically attenuate/suppress all HU-related changes, suggesting protective effects on muscle atrophy and decreased muscle oxidative capacity due to chronic neuromuscular inactivity.

Topics: Animals; Antioxidants; Dietary Supplements; Electric Stimulation; Hindlimb; Hindlimb Suspension; Male; Muscle, Skeletal; Muscular Atrophy; Oxidation-Reduction; Oxidative Stress; Rats; Rats, Sprague-Dawley; Reactive Oxygen Species; Xanthophylls

Extended periods of skeletal muscle disuse results in muscle atrophy and weakness. Currently, no therapeutic treatment is available for the prevention of this problem. Nonetheless, growing evidence suggests that prevention of disuse-induced oxidative stress in inactive muscle fibers can delay inactivity-induced muscle wasting. Therefore, this study tested the hypothesis that dietary supplementation with the antioxidant astaxanthin would protect against disuse muscle atrophy, in part, by prevention of myonuclear apoptosis. Wistar rats (8 weeks old) were divided into control (CT, n = 9), hindlimb unloading (HU, n = 9), and hindlimb unloading with astaxanthin (HU + AX, n = 9) groups. Following 2 weeks of dietary supplementation, rats in the HU and HU + AX groups were exposed to unloading for 7 days. Seven-day unloading resulted in reduced soleus muscle weight and myofiber cross-sectional area (CSA) by ~30 and ~47 %, respectively. Nonetheless, relative muscle weights and CSA of the soleus muscle in the HU + AX group were significantly greater than those of the HU group. Moreover, astaxanthin prevented disuse-induced increase in the number of terminal deoxynucleotidyl transferase dUTP nick end labeling (TUNEL)-positive nuclei. We conclude that astaxanthin supplementation prior to and during hindlimb unloading attenuates soleus muscle atrophy, in part, by suppressing myonuclear apoptosis.

Topics: Animals; Antioxidants; Apoptosis; Hindlimb Suspension; Male; Muscle, Skeletal; Muscular Atrophy; Oxidative Stress; Rats; Rats, Wistar; Xanthophylls

Astaxanthin is a carotenoid pigment and has been shown to be an effective inhibitor of oxidative damage. We tested the hypothesis that astaxanthin intake would attenuate immobilization-induced muscle atrophy in rats. Male Wistar rats (14-week old) were fed for 24 days with either astaxanthin or placebo diet. After 14 days of each experimental diet intake, the hindlimb muscles of one leg were immobilized in plantar flexion position using a plaster cast. Following 10 days of immobilization, both the atrophic and the contralateral plantaris muscles were removed and analyzed to determine the level of muscle atrophy along with measurement of the protein levels of CuZn-superoxide dismutase (CuZn-SOD) and selected proteases. Compared with placebo diet animals, the degree of muscle atrophy in response to immobilization was significantly reduced in astaxanthin diet animals. Further, astaxanthin supplementation significantly prevented the immobilization-induced increase in the expression of CuZn-SOD, cathepsin L, calpain, and ubiquitin in the atrophied muscle. These results support the postulate that dietary astaxanthin intake attenuates the rate of disuse muscle atrophy by inhibiting oxidative stress and proteolysis via three major proteolytic pathways.

Topics: Animals; Antioxidants; Male; Muscle, Skeletal; Muscular Atrophy; Oxidative Stress; Rats; Rats, Wistar; Reactive Oxygen Species; Restraint, Physical; Xanthophylls

A chronic decrease in neuromuscular activity (activation and/or loading) results in muscle atrophy and capillary regression that are due, in part, to the overproduction of reactive oxygen species. We have reported that antioxidant treatment with astaxanthin attenuates the overexpression of reactive oxygen species in atrophied muscles that, in turn, ameliorates capillary regression in hindlimb-unloaded rats. Astaxanthin supplementation, however, had little effect on muscle mass and fibre cross-sectional area. In contrast, intermittent loading of the hindlimbs of hindlimb-unloaded rats ameliorates muscle atrophy. Therefore, we hypothesized that the combination of astaxanthin supplementation and intermittent loading would attenuate both muscle atrophy and capillary regression during hindlimb unloading. As expected, 2 weeks of hindlimb unloading resulted in atrophy, a decrease in capillary volume and a shift towards smaller-diameter capillaries in the soleus muscle. Intermittent loading alone (1 h of cage ambulation per day) attenuated atrophy of the soleus, while astaxanthin treatment alone maintained the capillary network to near control levels. The combination of intermittent loading and astaxanthin treatment, however, ameliorated atrophy of the soleus and maintained the capillary volume and luminal diameters and the superoxide dismutase-1 protein levels near control values. These results indicate that intermittent loading combined with astaxanthin supplementation could be an effective therapy for both the muscle atrophy and the capillary regression associated with a chronic decrease in neuromuscular activity.

Topics: Animals; Antioxidants; Capillaries; Dietary Supplements; Hindlimb; Hindlimb Suspension; Male; Muscle, Skeletal; Muscular Atrophy; Rats; Rats, Sprague-Dawley; Xanthophylls

The capillary regression in skeletal muscles associated with a chronic decrease in activity is related to a dysfunction of endocapillary cells induced by over-expression of oxidative stress. We hypothesized that treatment with astaxanthin, an antioxidant, would attenuate the oxidative stress induced by decreased skeletal muscle use, and that this attenuation would prevent the associated capillary regression. The purpose of the present study was to investigate the antioxidant and preventive effects of astaxanthin on capillary regression in the soleus muscle during hindlimb unloading.. Twenty-four adult male Wistar rats were assigned randomly either to a control, control plus astaxanthin treatment, hindlimb unloaded or hindlimb unloaded plus astaxanthin treatment group for 7 days.. Hindlimb unloading resulted in a decrease in mean soleus absolute weight, capillary number, volume and luminal diameter. The accumulation of reactive oxygen species and the over-expression of superoxide dismutase (SOD-1), a decrease in the levels of vascular endothelial growth factor (VEGF) and its receptors, an inhibition of the angiopoietin pathway and an increase of thrombospondin-1 (TSP-1), as an anti-angiogenic factor were showed. Administration of astaxanthin attenuated the changes in SOD-1 and VEGF, up-regulated the angiogenic factors and reduced the capillary regression in the soleus of hindlimb unloaded rats. In addition, the VEGF-to-TSP1 ratio was higher in the astaxanthin treated groups than in the control and HU groups.. These results suggest that astaxanthin may be an effective treatment to counter the detrimental effects of a chronic decrease in skeletal muscle use on the capillary network and associated angiogenic pathways.

Topics: Animals; Antioxidants; Capillaries; Hindlimb Suspension; Male; Muscle, Skeletal; Muscular Atrophy; Rats; Rats, Wistar; Reverse Transcriptase Polymerase Chain Reaction; Xanthophylls