This study aimed to investigate the protective effect of enzymatically modified stevia (EMS) on C2C12 cell-based model of dexamethasone (DEX)-induced muscle atrophy to provide baseline data for utilizing EMS in functional health products. C2C12 cells with DEX-induced muscle atrophy were treated with EMS (10, 50, and 100 μg/mL) for 24 h. C2C12 cells were treated with EMS and DEX to test their effects on cell viability and myotube formation (myotube diameter and fusion index), and analyze the expression of muscle strengthening or degrading protein markers. Schisandra chinensis Extract, a common functional ingredient, was used as a positive control. EMS did not show any cytotoxic effect at all treatment concentrations. Moreover, it exerted protective effects on C2C12 cell-based model of DEX-induced muscle atrophy at all concentrations. In addition, the positive effect of EMS on myotube formation was confirmed based on the measurement and comparison of the fusion index and myotube diameter when compared with myotubes treated with DEX alone. EMS treatment reduced the expression of muscle cell degradation-related proteins Fbx32 and MuRF1, and increased the expression of muscle strengthening and synthesis related proteins SIRT1 and p- Akt/Akt. Thus, EMS is a potential ingredient for developing functional health foods and should be further evaluated in preclinical models.

A progressive muscle atrophy is strongly associated with aging, resulting in lower quality of life in elderly individuals. This study was conducted to determine relative hemoglobin (Hb) concentrations in the rabbit model of the sciatic nerve transection injury using non-invasive diffuse optical spectroscopy (DOS). From the 2nd week to the end of the experiment after sciatic nerve injury, a total muscle mass in nerve injured-group (NI group) significantly reduced compared with that in the normal group (p<0.001). During the capillary occlusion after nerve injury, the deoxy-hemoglobin (Hb-R) concentration in NI group significantly increased compared to that in the normal group at the 2nd and 3rd week after sciatic nerve injury (p<0.05). During the capillary release after nerve injury, the oxy-hemoglobin (Hb-O2) concentration in NI group significantly decreased at the 1st and 3rd week, and Hb-R significantly increased at 2nd week, compared to those in the normal group (p<0.05). Histological changes in the gastrocnemius muscle of NI group observed that clear fat filled spaces at the periphery of muscle fibers and angular fibers. From the results of this study, non-invasive DOS could be used to measure changes of Hb concentrations in muscles.

Amyotrophic lateral sclerosis (ALS) is progressive neurological disease that results in the death of motor neurons in the brain and spinal cord, leading to a decrease in skeletal muscle size and muscle weakness, wasting, or paralysis. Most research on ALS has focused on motor neuron death, and the underlying mechanisms are not well understood. This study examined the molecular mechanisms underlying muscle degeneration. We compared the protein and cytokine profiles of gastrocnemius muscle in ALS model hSOD1G93A mice at pre-symptomatic and symptomatic stages by western blotting. Pro-inflammatory factors including tumor necrosis factor-α, interleukin (IL)-1β and IL-6, and cluster of differentiation 11b were upregulated in the muscle of symptomatic as compared to pre-symptomatic mice. Additionally, the levels of oxidative stress-related proteins, heme oxygenase-1 and ferritin, were increased in muscle from symptomatic as compared to pre-symptomatic mice. We also observed increased autophagy dysfunction and metabolic dysregulation in the muscles of symptomatic hSOD1G93A as compared to non-Tg and pre-symptomatic hSOD1G93A mice, which was accompanied by upregulation of thrombospondin- 1, Prospero-related homeobox 1, glial fibrillary acidic protein, and DNA-damage-inducible 45α. Increased inflammation, oxidative stress, and autophagy contribute to motor neuron death and muscle atrophy in ALS, and the factors involved in these processes are potential therapeutic targets for treatment of this disease.

This study was conducted to investigate the effect of chronic alcohol supplementation on muscle atrophy in growing rats. Eighteen male Sprague Dawley rats were randomly divided into two groups: CG group (control group, n=9) and AG group (alcohol supplemented group, n=9). Alcohol group (3 g/kg BW) was orally supplemented every day. After the experimental period, serum components and muscle Akt, p-Akt, FoxO, p-FoxO, MuRF1, and P38 protein expressions were analyzed. In the results, the values of EDL and soleus muscle weights of AG group did not have significant differences compared to the value of the CG group. In the serum components, the value of the serum TG concentration of AG group was significantly increased compared to the value of the CG group. The value of the p-Akt/Akt and p-FoxO/FoxO of the AG group was significantly decreased compared to the value of the CG group (p<0.01). The MuRF1 protein expression of AG group was significantly increased compared to the value of the CG group (p<0.01). However, the values of p-P38/P38 between two groups did not have any significant difference. From these results, it was suggested that 4 weeks of chronic alcohol supplementation induced muscle atrophy via activated protein degradation pathway involving the inhibition of Akt phosphorylation and increased FoxO and MuRF1 protein expression of muscle in growing rats.

Muscle atrophy is characterized by a decrease in the mass of the muscle. With an increase in life expectancy and chronic illnesses, the incidence of muscle atrophy is increasing and the quality of life of patients is decreasing. Thus, reducing muscle atrophy is of high clinical and socio-economic importance. Mistletoe is a semi-parasitic plant that has been used as a traditional medicine in many countries to treat various human illnesses. It has been reported that Korean mistletoe extract (KME) has diverse biological functions including anti-tumor, anti-oxidant, anti-diabetic, anti-obesity properties, and extension of lifespan. Especially, we have recently reported that KME improves exercise endurance in mice, indicating its beneficial roles in enhancing the capacity of skeletal muscle. In this study, we investigated whether KME could activate the signaling pathway related to protein synthesis in a mouse model of muscle atrophy. Interestingly, KME efficiently activated the Akt/mTOR pathway, and Akt and mTOR are important signaling hub molecules for the acceleration of protein synthesis in muscle cells. In addition, KME also increased the activity of S6 kinase which is involved in the regulation of muscle cell size. Moreover, the ERK activity, required for transcription of ribosomal RNA for protein synthesis, was also enhanced in KME-treated mouse muscle. These data support the idea that KME increases muscle mass via increased protein synthesis. Our findings also suggest that Korean mistletoe might be a promising candidate for the development of functional foods that are beneficial for preventing muscle atrophy.

This study was designed to examine the effects of electroacupuncture and treadmill exercise on the improvement of muscle atrophy and Brain-Derived Neurotrophic Factor (BDNF) expression in an ischemic stroke model induced by middle cerebral artery occlusion. This study selected 120 Sprangue-Dawley rats, divided them into six groups, and assigned 5 rats to each group. Experiments were conducted for 1, 3 days and 1, 8 weeks, respectively. In each group, changes in weight of muscle and relative muscle of tibialis anterior muscle, histologic observations, and BDNF expression were observed and analyzed. For the changes in muscle weight of unaffected and affected sides of tibialis anterior, muscle atrophy was expressed in an affected side 3 days after ischemic stroke was induced. There was a statistically significant difference in Group VI 1 and 8 weeks after ischemic stroke was induced, compared to Group II (p<.05). For the changes in relative muscle weight of unaffected and affected sides of tibial anterior muscle, there was significant decrease in each group 3 days after ischemic stroke was induced, compared to Group I, while there was a statistically significant increase in Group VI 1 week after ischemic stroke was induced, compared to Group II (p<.05). For neurologic exercise behavior test, Group VI generally had the highest score, compared to other groups. The results of the behavior test suggests that 8 weeks after ischemic stroke was induced, Group VI improved in degeneration and inflammation of muscle fiber and decreased in destruction of nerve cells and cerebral infarction, thus indicating a similar state of muscle fiber and brain tissue in Group I. In immunohistochemical observations, Group 1 week showed increase in BDNF. Based on these results, electroacupuncture and treadmill exercise may improve muscle atrophy and change in BDNF expression of ischemic stroke rats and contribute to the improvement of exercise function.