• Biomedical Science Letters
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• v.10 no.3
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• pp.259-262
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• 2004

The aim of present study was to examine the effect of carrageenan on the tendon of skeletal muscle of rat. The tendon damage was induced by injection of carrageenan into skeletal hind muscle of rats. Rats were killed on 48 hours after carrageenan injection. The resulting tendons were fixed with 10％ neutral buffered formalin (NBF), dehydrated, embedded, sectioned by 4 μm, and stained by phosphotungstic acid hematoxylin (PTAH) or hematoxylin-eosin (H-E). Carrageenan induced the segregation of tendon fibers, intratendinous cleft, segregation of muscle cell group, wave arrangement of tendon fiber. The results suggest that carrageenan induced tendon damage of rat's skeletal muscle by morphological changes.

• Archives of Plastic Surgery
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• v.33 no.1
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• pp.31-38
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• 2006

The effect of melatonin on morphological changes after ischemia-reperfusion injury was investigated in rat skeletal muscle. Dimethyl-sulfoxide(DMSO) was also tested for comparison. Muscle injury was evaluated in 4 groups as a single laparotomy group(control), ischemia-reperfusion group, DMSO group, melatonin group. Left hind limb ischemia was induced for 4 hours by vascular clamping of the common femoral artery and followed by 24 hours of reperfusion. The midportion of gastrocnemius muscle was taken for histological evaluation. In light microscopic study, ischemia-reperfusion group showed severe neutrophil infiltration, interstitial edema, and partial loss or degeneration of muscle fibers. The muscle tissue of melatonin group showed relatively normal architecture with mild inflammatory cell infiltration. In electron microscopic study, dilated cisternae of sarcoplasmic reticulum, dilated mitochondria with electron loose matrix and dilated cristae, disordered or loss of myofilament, indistinct A-band and I-band, intracytoplasmic vacuoles, and markedly decreased glycogen granules were observed in ischemia-reperfusion group. But relatively well maintained A-band, I-band, Z-line, M-line, and mildly dilated mitochondria with well preserved cristae were observed in melatonin group. The DMSO group showed intermediately attenuated ultrastructural changes. The results show that melatonin improves morphologically ischemia-reperfusion injury more effectively than DMSO. In conclusion, melatonin seems to be a promising agent that can salvage the skeletal muscle from severe ischemia-reperfusion injury.

• 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.

• Archives of Plastic Surgery
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• v.32 no.6
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• pp.683-688
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• 2005

The ischemia-reperfusion injury of the skeletal muscles is caused by generation of reactive oxygen during ischemia and reperfusion. Melatonin or N-Acetyl-5-methoxy- tryptamine is suggested to have antioxidant effects in several tissues. In present study, we examined the protective effect of melatonin in a rat hind limb ischemia-reperfusion injury. Dimethyl-sulfoxide(DMSO) was also tested for comparison. Ischemia was induced for 4 hours by vascular clamping and followed by 1 hour or 24 hours of reperfusion. Muscle injury was evaluated in 4 groups such as single laparotomy group(control), ischemia-reperfusion group, DMSO group, melatonin group. Eedema ratio and malondialdehyde(MDA) of muscle tissue and serum level of creatine kinase(CK), were measeured at the end of reperfusion. DMSO and melatonin group showed significant amelioration of edema and serum CK compared with ischemia-reperfusion group. The decreasing effect was more prominent in melatonin group. The muscle tissue MDA concentration is significantly lower in melatonin group than in ischemia-reperfusion group. The results show that melatonin prevents and improves ischemia-reperfusion injury more effectively in a rat hind limb than DMSO dose. Thus, clinically the melatonin may be used for a beneficial treatment of such injuries

• Journal of Sericultural and Entomological Science
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• v.51 no.2
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• pp.123-129
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• 2013

The purpose of this study is to investigate the effects of supplementation of mulberry powder, mulberry extract and silkworm powder during the 8 weeks of resistance exercise on muscle increase of rats. Fifty males, Sprague-Dawley rat, were randomly divided into 5 groups: CON(control group, n = 10), REG(resistance exercise group, n = 10), MP REG(mulberry powder intake and resistance exercise group, n = 10), ME REG(mulberry extract intake and resistance exercise group, n = 10) and SP REG(silkworm powder intake and resistance exercise group, n = 10). After climbing the ladder without weights during the 1 week of adaptation period, the rats in the resistance exercise group were trained to climb a 0.98-m vertical(80 degree incline) ladder with weights in their tail during 7 weeks(10 times each day, 2 days per week). After exercise, the skeletal muscle was extracted from the flexor hallucis longus. The absolute weight of skeletal muscle was measured by the electronic balance and the relative weight of skeletal muscle about the weight was calculated. The strength and density of legs muscle were analyzed by the computed tomography scan. After 8 weeks of resistance exercise, the absolute weight of skeletal muscle wasn't significant, but it increased in MP REG 8%, ME REG 8% and SP REG 10% compared to REG. The relative weight of skeletal muscle increased significantly in SP REG compared to REG (p < 0.05). Additionally, there was a significant increase of density and strength of the forelegs in SP REG compared to CON (p < 0.05). However, there was no significant increase of density and strength of the hind legs. In conclusion, regular resistance exercise made rats muscle increase and there was more muscle increase effected by providing silkworm.

• Applied Microscopy
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• v.25 no.4
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• pp.26-51
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• 1995

The present study was designed to examine effect of long term weight-training on aging atrophy in the rat skeletal muscle. Male rats of 8, 15, and 24 month old were used. Each age groups included control and weight-training for 5 months by using body press apparatus. The histo- and cytochemical, ultrastructural and stereological changes in aging skeletal muscles of the rat were observed in the present study. During the training period the body weight and muscular weight in all groups except the rectus femoris and the gastrocnemius in young age groups remained constant, but muscular weights were increased in the rectus femoris and the gastrocnemius muscles in young age groups. In trained rat, the volume density of muscle fiber type IIA and IIB were increased, but those of type IIC was decreased. Type I remained constant in 8 and 15 month old age groups, but reduced in the tibialis anterior and the gastrocnemius muscles in the 24 month old groups. Some histotological and ultrastructural changes associated with age were found: numerical increase of cytiplasmic vacuoles, lysosomes, lipofuscins, and irregularity of myofibrils. At 24 month old groups some unusual formation of contraction band and muscle splitting were observed. After weight-training, ultrastructural degenerative changes occured in the type I muscle fiber, such as splitting of muscle fiber, disorganization of myofilaments, swelling of mitochondria, accumulation of many lipid droplets, appearance of many lysosomes and residual bodies and necrotic fibers, in the old age groups. But, in the type II muscle fibers hypertrophy of muscle fiber appeared without any noticible damage as the type I. The activities of $Mg^{++}$ -ATPase decreased with age and this enzyme activities in the trained rat were significantly decreased with age. Activities of the acid phosphatase were increased with age and significantly in the trained rat. In stereological analysis, volume density of the myofibrils and the tubular system were increased, on the other hand there mitochondrial capacity was decreased. These experimental results suggested that old rats are not susceptible to be affected by weight-training as young rats, and that physical capacity of the rats must be considered when old rats are exercised for training.

• The Korean Journal of Pharmacology
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• v.31 no.2
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• pp.207-217
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• 1995

To investigate the functional and immunological properties of the Ca-release channel in the sarcoplasmic reticulum(SR) of the eel skeletal muscle, $[^3H]ryanodine$ binding, SDS gel electrophoresis, $^{45}Ca\;release$ studies, and immunoblot assay were carried out in the SR of the eel skeletal muscle. Maximal binding sites(Bmax) and $K_D$ values of $[^3H]ryanodine$ for Ca-release channel of the SR of the eel skeletal muscle were $19.44{\pm}1.40\;pmole/mg$ protein and $15.55{\pm}1.69\;nM$, respectively. $[^3H]Ryanodine$ binding to RyR was increased by calcium and AMP. The SR of the eel skeletal muscle has two high molecular weight bands on the SDS PAGE. The mobility of upper band was more slower than the single band of the rabbit skeletal muscle, and that of the lower band was similar with the single band of canine cardiac muscle. Vesicular $^{45}Ca-release$ was activated by calcium. Ca-induced $^{45}Ca-release$ was significantly inhibited by $MgCl_2(2\;mM)$, ruthenium red$(10\;{/mu}M)$ or tetracaine(1 mM), but not by high concentration of calcium itself. AMP-induced $^{45}Ca-release$ was slightly occurred only in the absence of calcium, it was not inhibited by $MgCl_2$ or ruthenium red. Caffeine also increased $^{45}Ca-release$ from the SR vesicles, but it was not affected by $MgCl_2$ or ruthenium red. Polyclonal Ab against rat skeletal muscle RyR is reacted with that of rabbit, but not reacted with that of the eel skeletal muscle. These results suggested that ryanodine receptor of the SR of the eel skeletal muscle is showing some similar properties with that of mammalian skeletal muscle, but might be an another isotype channel having two bands which is less sensitive to AMP, not cross-reacted with antisera against rat RyR, and not inhibited by high concentration of calcium.

• Herbal Formula Science
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• v.24 no.3
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• pp.153-161
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• 2016

Chronic alcoholic myopathy is one of the most common skeletal muscle disorders. It is characterized by a reduction in the entire skeletal musculature, skeletal muscle weakness, and difficulties in gait. Patients with alcoholic hepatitis and cirrhosis have severe muscle loss that contributes to worsening outcome. Although the myopathy selectively affects Type II (fast twitch, glycolytic, anaerobic) skeletal muscle fibers, total skeletal musculature is reduced. The severity of the muscle atrophy is proportional to the duration and amount of alcohol consumed and leads to decreased muscle strength. The mechanisms for the myopathy are generally unknown but it is not due to overt nutritional deficiency, nor due to either neuropathy or severe liver disease. Skeletal muscle mass and protein content are maintained by a balance between protein synthesis and breakdown and in vivo animal models studies have shown that ethanol inhibits skeletal muscle protein synthesis. Daekumeumja is a traditional Korean medicine that is widely employed to treat various alcohol-induced diseases. Muscle diseases are often related to liver diseases and conditions. The main objective of this study was to assess that Daekumeumja extract could have protective effect against alcoholic myopathy in a Sprague-Dawley rat model. Rats were orally given 25% ethanol (5ml/kg, body weight) for 8 weeks. After 30 minutes, rats were administrated with Daekumeumja extract. Controls were similarly administrated with the vehicle alone. The weights of gastrocnemius, soleus and plantaris muscles were assessed and the morphologic changes of gastrocnemius and plantaris muscles were also assessed by hematoxylin and eosin staining. In results, The muscles from ethanol treated rats displayed a significant reduction in muscle weight and average cross section area compared to Normal group. Daekumeumja extract treated group showed increased muscle weight and muscle fiber compared to the ethanol treated group. It was concluded that Daekumeumja extract showed ameliorating effects on chronic alcohol myopathy in skeletal muscle.

• The Journal of Korean Physical Therapy
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• v.19 no.4
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• pp.1-14
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• 2007

Background: It is generally accepted that skeletal muscle contraction is triggered by nerve impulse and intracellular $Ca^{2+}\;([Ca^{2+}]_i)$ released from intracellular $Ca^{2+}$ stores such as sarcoplasmic reticulum (SR). Specifically, this process, called excitation-contraction (E-C) coupling, takes place at intracellular junctions between the plasma membrane, the transverse (T) tubule L-type $Ca^{2+}$ channel (dihydropyridine-sensitive L-rype $Ca^{2+}$ channel, DHPR, also called tetrads), and the SR $Ca^{2+}$ release channel (ryanodine-sensitive $Ca^{2+}$ release channel, RyR, also called feet) of internal $Ca^{2+}$ stores in skeletal muscle cells. Furthermore, it has been reported that the $Ca^{2+-}$ dependent and -independent contraction determine the expression of skeletal muscle genes, thus providing a mechanism for tightly coupling the extent of muscle contraction to regulation of muscle plasticity-related excitation-transcription (E-T) coupling. Purpose: Expression and activity of plasticity-associated enzymes in gastrocnemius muscle strips have not been well studied, however. Methods: Therefore, in this study the expression and phosphorylation of E-C and E-T coupling-related mediators such as protein kinases, ROS(reactive oxygen species)- and apoptosis-related substances, and others in gastrocnemius muscles from rats was examined. Results: I found that expression and activity of MAPKs (mitogen-activated protein kinases, ERK1/2, p38MAPK, and SAPK/JNK), apoptotic proteins (cleaved caspase-3, cytochrome c, Ref-1, Bad), small GTP-binding proteins (RhoA and Cdc42), actin-binding protein (cofilin), PKC (protein kinase C) and $Ca^{2+}$ channel (transient receptor potential channel 6, TRPC6) was observed in rat gastrocnemius muscle strips. Conclusion: These results suggest that MAPKs, ROS- and apoptosis-related enzymes, cytoskeleton-regulated proteins, and $Ca^{2+}$ channel may in part functionally import in E-C and E-T coupling from rat skeletal muscles.

• Archives of Pharmacal Research
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• v.19 no.6
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• pp.497-501
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• 1996

A gene coding for triosephosphate isomerase (TPI) from a rat skeletal muscle cDNA library was cloned and its nucleotide sequence was determined. The 1, 348-bp cDNA clone contains 24 bp $5^I$ noncoding region, the entire 750 bp coding region corresponding to a protein of 249 amino acids, $547bp 3^I$ noncoding region and part of a poly(A) tail. It also contains a polyadenylation signal, AATAAA, starting from 17 bp upstream of the poly(A) tail. The calculated molecular weight of rat TPI is 27.8 kDa and the net charge is +4. The deduced amino acid sequence from rat TPI CDNA sequence has 93% and 94% homology with that of mouse and human clones, respectively. The amino acids at the residue of Asn12, Lys14, His96, Glu 166, His96, His101, Ala177, Tyr165, Glu13O, Tyr2O9, and Ser212 in catalytic site are completely identical, confirming that the functional residues in TPI proteins are highly conserved throughout evolution. The most profound characteristic of rat TPI enzyme, compared with other TPIs, is that there are five cysteine substitutions at the residue of 21, 27, 159, 195 and 204. A Glu123 instead of Gly was found in rabbit, rhesus, mouse and human sequences. Through the method of RT-PCR, the mRNA transcription level of TPI gene was found to be different among various tissues and was highest in muscle.