• Journal of Physiology & Pathology in Korean Medicine
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• v.22 no.6
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• pp.1454-1461
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• 2008

In oriental medicine, it is known that Eucommiae Cortex (EC) has strengthening and rehabilitative effects on the bone-muscle dysfunction. This study aimed to evaluate the effect of EC on the skeletal muscle atrophy. The muscle atrophy was induced by unilateral transection of the sciatic nerve in Sprague-Dawley rats. EC (water-extract, 170mg/100 g body weight) was treated once a day for 12 days. In this study, the effect of EC examined the muscle weight of hind limb, cross section areas of muscle fibers, fiber type compositions, apoptosis related factors (Bax and Bcl-2). EC reduced muscle atrophy in soleus (SOL), medial gastrocnemius (MGT), extensor digitorum longus, and tibialis posterior significantly in the damaged hind limb. EC increased type-I muscle fibers and decreased type-II muscle fibers significantly in SOL of the damaged hind limb. EC enlarged cross section areas of type-I and type-II muscle fibers significantly in SOL. EC enlarged cross section areas of type-I and type-II muscle fibers significantly in. EC reduced apoptotic nuclei and atrophic muscle fibers in SOL and MGT. EC reduced Bax positive muscle nuclei in SOL and MGT. EC up-regulated Bcl-2 positive muscle fibers in SOL and MGT. These results suggest that EC has an anti-atrophic effect and anti-apoptotic effect against myonuclear apoptosis induced by the peripheral nerve damage.

• 대한상한금궤의학회지
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• v.4 no.1
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• pp.67-74
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• 2012

Objective : This research is to prove the effectiveness of Jinmutang in curing muscular atrophy Method : To achieve the goal of this research, we gave Jinmutang to the selected patients and observed the progress. Results & Conclusions: The results indicate the followings 1. After the treatment with Jinmu-tang, the symptoms of muscular atrophy were significantly improved. 2. JinmuTang based on sanghanron, as shown in the example above, has an effect on Muscle atrophy of the legs, But we need to study this pharmacologic and biological mechanism.

• Journal of Ginseng Research
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• v.47 no.6
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• pp.726-734
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• 2023

Background: Skeletal muscles play a key role in physical activity and energy metabolism. The loss of skeletal muscle mass can cause problems related to metabolism and physical activity. Studies are being conducted to prevent such diseases by increasing the mass and regeneration capacity of muscles. Ginsenoside Rg5 has been reported to exhibit a broad range of pharmacological activities. However, studies on the effects of Rg5 on muscle differentiation and growth are scarce. Methods: To investigate the effects of Rg5 on myogenesis, C2C12 myoblasts were induced to differentiate with Rg5, followed by immunoblotting, immunostaining, and qRT-PCR for myogenic markers and promyogenic signaling (p38MAPK). Immunoprecipitation confirmed that Rg5 increased the interaction between MyoD and E2A via p38MAPK. To investigate the effects of Rg5 on prevention of muscle mass loss, C2C12 myotubes were treated with dexamethasone to induce muscle atrophy. Immunoblotting, immunostaining, and qRT-PCR were performed for myogenic markers, Akt/mTOR signaling for protein synthesis, and atrophy-related genes (Atrogin-1 and MuRF1). Results: Rg5 promoted C2C12 myoblast differentiation through phosphorylation of p38MAPK and MyoD/E2A heterodimerization. Furthermore, Rg5 stimulated C2C12 myotube hypertrophy via phosphorylation of Akt/mTOR. Phosphorylation of Akt induces FoxO3a phosphorylation, which reduces the expression of Atrogin-1 and MuRF1. Conclusion: This study provides an understanding of how Rg5 promotes myogenesis and hypertrophy and prevents dexamethasone-induced muscle atrophy. The study is the first, to the best of our knowledge, to show that Rg5 promotes muscle regeneration and to suggest that Rg5 can be used for therapeutic intervention of muscle weakness and atrophy, including cancer cachexia.

• Journal of Korean Academy of Nursing
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• v.39 no.3
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• pp.393-400
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• 2009

Purpose: The purpose of this study was to examine the effects of unilateral sciatic nerve injury on unaffected hindlimb muscles of rats. Methods: Adult male Sprague-Dawley rats were assigned to one of three groups: control(C) group(n=10) that had no procedures, sham(S) group(n=10) that underwent sham left sciatic nerve transection, and sciatic nerve transection(SNT) group(n=9) that underwent left sciatic nerve transection. At 15 days rats were anesthetized, and the soleus, plantaris and gastrocnemius muscles were dissected. Results: Muscle weight of the unaffected plantaris muscle in the SNT group was significantly lower than in the other two groups. Type II fiber cross-sectional areas of the unaffected plantaris and gastrocnemius muscles in the SNT group were significantly smaller than in the other two groups. The decrease of muscle weights and Type I, II fiber cross-sectional areas of the unaffected three muscles in the SNT group were significantly less than that of the affected three muscles. Conclusion: Hindlimb muscle atrophy occurs in the unaffected side after unilateral sciatic nerve injury, with changes in the plantaris and gastrocnemius muscle being more apparent than changes in the soleus muscle. These results have implications for nursing care, in the need to assess degree of muscle atrophy in unaffected muscles as well as affected muscles.

• Biomedical Science Letters
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• v.29 no.3
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• pp.190-200
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• 2023

Skeletal muscle, essential for metabolism, thermoregulation, and immunity, undergoes myogenic differentiation that results in myotube formation. Trans-anethole (TA), the major constituent in essential oil produced by anise, star anise, and fennel, whose function in skeletal muscle has not yet been elucidated. Therefore, we investigated whether TA influenced muscle differentiation in mouse C2C12 myoblasts. Cells were induced to differentiate using a differentiation medium with or without TA (50 or 200 mg/mL) daily for 5 days. We measured myotube length and diameter after differentiation days 1, 3, and 5 and analyzed the expression of myogenic markers (myoblast determination protein 1, myogenin, myocyte enhancer factor 2, muscle creatine kinase, and myosin heavy chain) and atrophy-related genes (atrogin-1 and muscle ring finger-1 [MuRF-1]) using quantitative real-time PCR. Additionally, we observed the expression of total protein kinase B (Akt) and phosphorylated Akt (p-Akt) using western blotting. Our data showed that TA significantly induced the formation of smaller and thinner myotubes and reduced the myogenic factor expression. Furthermore, the atrogin-1 and MuRF-1 expression markedly increased by TA. Consistent with these findings, TA significantly decreased the expression of total Akt and p-Akt. Taken together, these results indicate that TA inhibits myogenic differentiation of C2C12 cells via reduction of both total Akt and p-Akt. Our findings may provide valuable insights into the impact of PAA on individuals at risk of muscle atrophy.

• Journal of Biomedical Engineering Research
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• v.38 no.4
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• pp.175-182
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• 2017

Microcurrent electrical stimulation(MES) has been used to accelerate recovery of atrophied skeletal muscle. However, convincing stimulation parameters for suppressing muscle atrophy due to injured sciatic nerve remains unclear. The objective of this study was to investigate the effective intensity of MES on restraining muscle atrophy with rat model underwent sciatic nerve injury(SNI). Twenty-5-week-old Sprague Dawley male rats were equally assigned to five groups : Control group(Control, CON, n = 4), Denervation group(Denervation, D, n = 4), Denervation with MES of $22{\mu}A$ group(Denervation + $22{\mu}A$, D+22, n = 4), Denervation with MES of $100{\mu}A$ group (Denervation + $100{\mu}A$, D+100 n = 4), Denervation with MES of $400{\mu}A$ group(Denervation + $400{\mu}A$, D+400, n = 4). To induce muscle atrophy, all rats in the D, D+22, D+100, and D+400 groups, were subjected to sciatic nerve injury on their right hindlimb and allowed to have 1 week of resting period. Following this period, rats underwent daily MES(60 min/ a day, 5times/1week) for 4 weeks. After that, we investigate morphological changes in muscle volume by using in vivo micro-computed tomography at week 0, 1, 3 and 5. After 5 weeks, the muscle volume had the highest value in D+400 group, and also noticeably increased in D+100 group compared to it in D group. The results of this study imply that MES with current intensities between $100-400{\mu}A$ can suppress muscle atrophy effectively.

• Journal of Ginseng Research
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• v.46 no.3
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• pp.454-463
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• 2022

Background: Gintonin-enriched fraction (GEF), a non-saponin fraction of ginseng, is a novel glycolipoprotein rich in hydrophobic amino acids. GEF has recently been shown to regulate lipid metabolism and browning in adipocytes; however, the mechanisms underlying its effects on energy metabolism and whether it affects sarcopenic obesity are unclear. We aimed to evaluate the effects of GEF on skeletal muscle atrophy in high-fat diet (HFD)-induced obese mice. Methods: To examine the effect of GEF on sarcopenic obesity, 4-week-old male ICR mice were used. The mice were divided into four groups: chow diet (CD), HFD, HFD supplemented with 50 mg/kg/day GEF, or 150 mg/kg/day GEF for 6 weeks. We analyzed body mass gain and grip strength, histological staining, western blot analysis, and immunofluorescence to quantify changes in sarcopenic obesity-related factors. Results: GEF inhibited body mass gain while HFD-fed mice gained 22.7 ± 2.0 g, whereas GEF-treated mice gained 14.3 ± 1.2 g for GEF50 and 11.8 ± 1.6 g for GEF150 by downregulating adipogenesis and inducing lipolysis and browning in white adipose tissue (WAT). GEF also enhanced mitochondrial biogenesis threefold in skeletal muscle. Furthermore, GEF-treated skeletal muscle exhibited decreased expression of muscle-specific atrophic genes, and promoted myogenic differentiation and increased muscle mass and strength in a dose-dependent manner (p < 0.05). Conclusion: These findings indicate that GEF may have potential uses in preventing sarcopenic obesity by promoting energy expenditure and attenuating skeletal muscle atrophy.

• Journal of The Korean Society of Integrative Medicine
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• v.11 no.1
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• pp.63-70
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• 2023

Purpose : Excessive alcohol causes damage to skeletal muscles, leading to the development of a specific disease entity called alcoholic myopathy. Chronic inflammation is related as an underlying mechanism for the loss of muscle mass induced by alcohol. Pro-inflammatory cytokines such as TNF-α (tumor necrosis factor-α) and IL-6 (interleukin-6) play a role in this process. The acupuncture point Feng Shi (GB 31) is located on the midline of the lateral aspect of the thigh, above the transverse popliteal crease. This acupoint is used for the treatment of weakness, atrophy, numbness, and post-stroke symptoms of lower limbs. The purpose of this study was to investigate the effect of Feng Shi stimulation on muscle atrophy caused by chronic alcohol administration. Method : Young male Sprague-Dawley rats were randomly divided into three groups of eight each: Normal, Control, and GB31. The rats in the Control and GB31 groups were orally given 25 % ethanol (5 ㎖/kg, body weight) daily for 4 weeks. The Normal group was similarly administered saline. The acupressure at Feng Shi was treated to rats in the GB31 group. After 4 weeks, the body weight, muscle weight and cross-sectional area of gastrocnemius were assessed and the histological changes in gastrocnemius muscle fiber were observed by hematoxylin and eosin staining. Moreover, TNF-α and IL-6 expressions were immunohistochemistrically evaluated. Results : Acupressure stimulation at Feng Shi had a protective effect on the weight reduction of the gastrocnemius muscle caused by alcohol intake, and had an effect of suppressing anatomical change in muscle fiber and decreasing the average cross-sectional area. Also, the immunoreactivities of TNF-α and IL-6 in the GB31 group were decreased. Conclusion : These results suggest that acupressure at Feng Shi has protective effects on chronic alcohol-induced muscle atrophy by inhibiting pre-inflammatory proteins such as TNF-α and IL-6.

• Physical Therapy Korea
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• v.14 no.1
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• pp.1-10
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• 2007

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.

• Journal of Applied Biological Chemistry
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• v.65 no.4
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• pp.387-396
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• 2022

Skeletal muscle accounts for about 40-50% of body weight and is an important tissue that performs various functions, such as maintaining posture, supporting soft tissues, maintaining body temperature, and respiration. Cancer, which occurs widely around the world, causes cancer cachexia accompanied by muscular atrophy, which reduces the effectiveness of anticancer drugs and greatly reduces the quality of life and survival rate of cancer patients. Therefore, research to improve cancer cachexia is ongoing. However, there are few studies on the link between cancer and muscle atrophy. Cancer cells exhibit distinct microenvironment and metabolism from tumor cells, including tumor-associated macrophages (TAM), tumor-associated neutrophils (TAN), and insulin resistance due to the Warburg effect. Therefore, we summarize the microenvironment and metabolic characteristics of cancer cells, and the molecular mechanisms of muscle atrophy that can be affected by cytokine and insulin resistance. In addition, this suggests the possibility of improving cancer cachexia of substances affecting TAM, TAN, and Warburg effect. We also summarize the mechanisms identified so far through single agents and the signaling pathways mediated by them that may ameliorate cancer cachexia.