• The Korean Journal of Food And Nutrition
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• v.30 no.2
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• pp.371-377
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• 2017

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.

• Journal of Oral Medicine and Pain
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• v.47 no.4
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• pp.217-221
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• 2022

Neurogenic muscular atrophy is muscle wasting and weakness caused by trauma or disease of the nerve that innervates the muscle. We describe a case of unilateral trigeminal neuropathy and neurogenic muscular atrophy of the masticatory muscle caused by a tumor in the foramen ovale. A 59-year-old man visited our clinic complaining of difficulty in right-sided mastication. There were no evident clinical signs and symptoms of temporomandibular disorder. However, severe atrophy of the right masseter and temporalis muscles and hypesthesia of the right side mandibular nerve area were confirmed. Through T1 and T2 signals on magnetic resonance imaging (MRI), a mass suspected of a neurogenic tumor was observed in the foramen ovale and cavernous sinus. Severe atrophy of all masticatory muscles on the right side was observed. This rare case shows trigeminal neuropathy caused by a tumor around the foramen ovale and atrophy of the ipsilateral masticatory muscles. For an accurate diagnosis, it is essential to identify the underlying cause of muscle atrophy with neurologic symptoms present. This can be done through a more detailed clinical examination, including sensory testing and brain MRI, and consider a referral to neurology or neurosurgery for the differential diagnosis of the intracranial disorder.

• Journal of Physiology & Pathology in Korean Medicine
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• v.23 no.2
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• pp.405-411
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• 2009

This study evaluated the effects of Puerariae Radix on the skeletal muscle atrophy, Muscle atrophy was induced by the sciatic nerve transection in Sprague-Dawley rats, then aqueous-extract of Puerariae Radix was administered for 12 days, Muscle wet weight was measured in soleus, plantaris, and medial gastrocnemius. Muscle fiber type was classified by MHCf immunohistochemistry. Muscle fiber type proportion and cross section area of muscle fiber also was observed in medial gastrocnemius. Bax and Bcl-2 expressions in medial gastrocnemius of the damaged hind limb were evaluated with immunohistochemistry. The results are as follows; Puerariae Radix attenuated muscle atrophy in soleus of the sciatic nerve transectioned rats, but there was statistic significance. Puerariae Radix attenuated significantly atrophy in plantaris at 12 days and in medial gastrocnemius at 8 days and 12 days. Puerariae Radix improved histology of the atrophic changes and increased significantly cross section areas of type-I and type-II muscle fibers in medial gastrocnemius of the sciatic nerve transectioned rats. Puerariae Radix did not affect to muscle fiber type proportion in medial gastrocnemius of the sciatic nerve transectioned rats. Puerariae Radix attenuated significantly Bax positive nuclei but did not affect to Bcl-2 positive muscle fibers in medial gastrocnemius of the sciatic nerve transectioned rats.According to above results, Puerariae Radix may have an anti-atrophy effect on the denervated skeletal muscle through anti-apoptotic effects on muscle fibers.

• Korean Journal of Exercise Nutrition
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• v.23 no.3
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• pp.45-49
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• 2019

[Purpose] Recent studies suggest that ursolic acid (UA) is a potential candidate for a resistance exercise mimetic that can increase muscle mass and alleviate the deleterious effect of skeletal muscle atrophy on bone health. However, these studies evaluated the effects of UA on skeletal muscle and bone tissues, and they have not verified whether such effect could occur concurrently on muscle and bone, as is the case with resistance exercise. Thus, the aim of this study was to analyze the effect of UA injection on muscle mass and bone microstructure using an animal model of atrophy to demonstrate the potential of UA as a resistance exercise mimetic. [Methods] The immobilization (IM) method was used on the left hindlimb of Sprague Dawley (SD) rats for 10 days to induce muscle atrophy, whereas the right hindlimb was used as an internal control (IC). The animal models were divided into two groups, SED (sedentary, n=6) and UA (n=6) to demonstrate the effect of UA on atrophic skeletal muscles. The UA group received a daily intraperitoneal injection of UA (5 mg/kg/day) for 8 weeks. After 10 days of IM, the data collected for the IC were compared with that of IM to determine whether muscle atrophy might occur. [Results] Muscle atrophy was induced and bone mineral density (BMD) decreased significantly. The 8-week UA treatment significantly increased the gastrocnemius muscle mass compared to the SED group. In regard to the effect of UA on bones, negative results such as a decrease in BMD, trabecular bone volume fraction, and trabecular number, and an increase in trabecular separation, were observed in the SED group, but no such difference was observed in the UA group. No significant difference was observed in atrophic hindlimbs between SED and UA groups. [Conclusion] These results alone are insufficient to suggest that UA is a potential resistance exercise mimetic for atrophic skeletal muscle and weakened bone. However, this study will help determine the potential of UA as a resistance exercise mimetic.

• The Journal of Churna Manual Medicine for Spine and Nerves
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• v.3 no.2
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• pp.61-68
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• 2008

Objectives : Lumbar multifidus muscle stabilize lumbar spine. Atrophy of multifidus muscle follows disfunction of low back pain patient's activity and increase the reoccurency of herniation of nucleus purposus surgery. Lumbar herniation of nucleus purposus if common cause of low back pain. We have evaluated the atrophy of multifidus of nucleus purposus. Methods : Five patients were diagnosed as Lumbar herniation of nucleus purposus through the CT imaging. CT imaging were visually analysed to know lumbar multifidus muscle atrophy. Results and Conclusions : Examination of multifidus muscle atrophy should be considered with assessing CT imaging of lumbar spine. It may help for further evaluation and planning the treatment of Lumbar herniation of nucleus purposus patient.

• Journal of Korean Medicine Rehabilitation
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• v.27 no.4
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• pp.1-9
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• 2017

Objectives Oxidative stress, in which antioxidant proteins and scavenger protection are overwhelmed by reactive oxygen species (ROS) production, is recognized as one of central causes of disuse muscle atrophy. In this study, the hypothesis that oral treatment with Dangguibohyul-tang (Dangguibuxuetang) could attenuate immobilization-induced skeletal muscle atrophy was tested. Methods The hindlimb immobilization was performed with casting tape to keep the left ankle joint in a fully extended position. The Rats in Dangguibohyul-tang treated group (DGBHT) (n=10) were orally administrated Dangguibohyul-tang water extract, and rats of Control group (n=10) were given with saline only. After 2 weeks of immobilization, the morphology of right and left gastrocnemius muscles in both DGBHT and Control groups were assessed by hematoxylin and eosin staining. Results Dangguibohyul-tang water extract represented the significant protective effects against the reductions of the left gastrocnemius muscles weight and average cross section area to compared with Control group. Moreover, the treatment with Dangguibohyul-tang extract significantly enhanced the Cu/Zn-SOD activities in gastrocnemius muscle compared with Control group. Conclusions Thses results suggest that Dangguibohyul-tang has protective effects against immobilization-induced muscle atrophy by increasing the Cu/Zn-SOD activities in gastrocnemius muscle.

• The Korean Journal of Physiology and Pharmacology
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• v.13 no.6
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• pp.491-496
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• 2009

Skeletal muscle atrophy is a common phenomenon during the prolonged muscle disuse caused by cast immobilization, extended aging states, bed rest, space flight, or other factors. However, the cellular mechanisms of the atrophic process are poorly understood. In this study, we investigated the involvement of mitogen-activated protein kinase (MAPK) in the expression of muscle-specific RING finger 1 (MuRF1) during atrophy of the rat gastrocnemius muscle. Histological analysis revealed that cast immobilization induced the atrophy of the gastrocnemius muscle, with diminution of muscle weight and cross-sectional area after 14 days. Cast immobilization significantly elevated the expression of MuRF1 and the phosphorylation of p38 MAPK. The starvation of L6 rat skeletal myoblasts under serum-free conditions induced the phosphorylation of p38 MAPK and the characteristics typical of cast-immobilized gastrocnemius muscle. The expression of MuRF1 was also elevated in serum-starved L6 myoblasts, but was significantly attenuated by SB203580, an inhibitor of p38 MAPK. Changes in the sizes of L6 myoblasts in response to starvation were also reversed by their transfection with MuRF1 small interfering RNA or treatment with SB203580. From these results, we suggest that the expression of MuRF1 in cast-immobilized atrophy is regulated by p38 MAPK in rat gastrocnemius muscles.

• Journal of Korean Medicine Rehabilitation
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• v.19 no.4
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• pp.151-163
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• 2009

Objectives : In the assessment of the lumbar spine by magnetic resonance imaging (hereinafter, "MRI"), changes in the paraspinal muscles are overlooked. The purpose of our study is to examine the correlation between the multifidus muscle atrophy on MRI findings and the clinical findings in low back pain (hereinafter, "LBP") patients. Methods : The retrospective study on 38 LBP patients, presenting either with or without associated leg pains, was undertaken. The MRI findings on the patients were visually analysed to find out a lumbar multifidus muscle atrophy, disc herniation, disc degeneration, spinal stenosis and nerve root compressions. The clinical history in each case was obtained from their case notes and pain drawing charts. Results : The lumbar multifidus muscle atrophy has occurred from more than 80% of the patients with LBP. Most of lumbar multifidus muscle atrophies have increased from lower level of lumbar spine. It was bilateral in the majority of the cases. In addition, multifidus muscle atrophy was correlated to the patient's age, disc degenerations and spinal stenosis. On the contrary, gender, the duration of LBP, referred leg pain, disc herniation and nerve root compressions had no relevance to multifidus muscle atrophies. Therefore, when assessing the MRIs of the lumbar spine, we should have more attetion on multifidus muscle, because it has lot's of information about spinal neuropathy problems. Conclusions : Therefore, the examination of multifidus muscle atrophies should be considered when assessing the MRIs of the lumbar spine. In addition, it helps to evaluate and plan the treatment modalities of LBP. Moreover, it prevents from LBP by discovering the importance between the multifidus muscle and the spine stabilization exercise.

• Journal of Microbiology and Biotechnology
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• v.28 no.4
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• pp.520-526
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• 2018

Conessine, a steroidal alkaloid, is a potent histamine H3 antagonist with antimalarial activity. We recently reported that conessine treatment interferes with $H_2O_2$-induced cell death by regulating autophagy. However, the cellular signaling pathways involved in conessine treatment are not fully understood. Here, we report that conessine reduces muscle atrophy by interfering with the expression of atrophy-related ubiquitin ligases MuRF-1 and atrogin-1. Promoter reporter assay revealed that conessine treatment inhibits FoxO3a-dependent transcription, $NF-{\kappa}B$-dependent transcription, and p53-dependent transcription. We also showed by quantitative RT-PCR and western blot assays that conessine treatment reduced dexamethasone-induced expression of MuRF1 and atrogin-1. Finally, we demonstrated that conessine treatment reduced dexamethasone-induced muscle atrophy using differentiated C2C12 cells. These results collectively suggest that conessine is potentially useful in the treatment of muscle atrophy.

• Korean Journal of Poultry Science
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• v.49 no.4
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• pp.265-272
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• 2022

Many studies on poultry have been conducted in the poultry industry to improve their important economic traits, such as egg production, meat quality, and carcass yield. Environmental changes affect the poultry's economic traits, including muscle growth. The purpose of this study is to investigate the mechanisms by which simvastatin causes muscle injury in quail muscle cells. Following treatment with various doses of simvastatin, LD50 in the quail myoblast cells was determined using a cell viability test; cell death was caused by apoptosis and/or necrosis. Thereafter, the expression patterns of the atrophy marker genes were examined via quantitative reverse-transcription polymerase chain reaction (qRT-PCR). The results showed that the transcriptional levels of the muscle atrophy marker genes (Atrogin-1, TRIM63) and the upstream genes in their signaling cascade were increased by simvastatin treatment. This indicated that simvastatin induced myogenic cell death and muscle injury via protein degradation through muscle atrophy signaling. Further studies should focus on identifying the mechanism by which simvastatin induces the protein degradation signaling pathway in quail muscle..