PURPOSE: The purpose of this study was to examine the effect of anorexia and neuropathic pain induced by cisplatin on hindlimb muscles of rats. METHODS: Adult male Sprague-Dawley rats were divided into two groups, a cisplatin-treated group (n=10) and a control group (n=10). In the cisplatin-treated group, cisplatin at a dose of 2 mg/kg was injected intraperitoneally two times a week up to a cumulative dose of 20 mg/kg over 5 weeks, and in the control group saline (0.9% NaCl) was injected intraperitoneally at the same dose and duration as the cisplatin-treated group. At 34 days all rats were anesthetized, after which the soleus and plantaris muscles were dissected. Withdrawal threshold, body weight, food intake, activity, muscle weight, Type I and II fiber cross-sectional areas and myofibrillar protein content of the dissected muscles were determined. RESULTS: Compared with the control group, the cisplatin-treated group showed significant decreases (p<.05) in withdrawal threshold, activity, food intake, body weight, Type I and II fiber cross-sectional areas, myofibrillar protein content and weight of the soleus and plantaris muscles. CONCLUSION: Muscular atrophy in hindlimb occurs due to anorexia and neuropathic pain induced by the cisplatin treatment.
Animals ; *Anorexia ; Body Weight ; Cisplatin/*toxicity ; Eating ; Hindlimb ; Injections, Intraperitoneal ; Male ; Motor Activity ; Muscle Fibers, Skeletal/metabolism/pathology ; Muscle Proteins/metabolism ; Muscle, Skeletal/*drug effects/physiology ; Neuralgia/*chemically induced/pathology ; Rats ; Rats, Sprague-Dawley

The troponin I subunit (TnI) was used as a molecular marker to explore the relationship between the resting intracellular Ca(2+) concentration and myofibril degradation in muscle fibers. The isolated soleus muscle strips of rats were treated by caffeine and H2O2. Caffeine is an opener to increase the calcium release channel open probability of sarcoplasmic reticulum (SR) in contraction phase. H2O2 induces a calcium leak of SR calcium release channel in relaxation phase. The expression and degradation of TnI were detected by Western blot. The resting tension of tetanic contraction and expression of TnI were not changed, but the developed tension was lowered in isolated soleus muscle strips during 40 min of calcium-free Krebs perfusion. Low concentrations of caffeine (1 and 5 mmol/L) perfusion induced a transient increase in resting tension during fatigue period, but did not alter the extent of fatigue, recovery rate after fatigue and expression of TnI in muscle strips. High concentration of caffeine (10 mmol/L) perfusion induced a progressive increase in resting tension, a higher rate of fatigue and a decrease in recovery rate after fatigue in muscle strips. There was a detectable degradation of TnI in soleus after 10 mmol/L caffeine treatment. H2O2 perfusion facilitated a progressive increase in resting tension in a dose-dependent manner, but did not influence the fatigue rate of tetanic contraction. The recovery rate after fatigue showed a quick resumption before decline during H2O2 perfusion. Degradation of TnI occurred in 5 and 10 mmol/L H2O2-treated soleus muscles. Since resting tension is dependent on intracellular Ca(2+) concentration, the above-mentioned results suggest that SR Ca(2+) leakage in relaxation phase may induce a degradation of TnI in skeletal muscle fibers.
Animals ; Caffeine ; pharmacology ; Calcium ; metabolism ; Calcium Channels ; metabolism ; Hydrogen Peroxide ; pharmacology ; In Vitro Techniques ; Muscle Fibers, Skeletal ; metabolism ; Rats ; Sarcoplasmic Reticulum ; pathology ; Troponin I ; metabolism

OBJECTIVE: To study the mRNA expression of muscle phenotype and collagen of soft palate and pathology in obstructive sleep apnea hypopnea syndrome (OSAHS). METHOD: We used the Real-time PCR to test the mRNA expression of soft palate muscle myosin heavy chain (MyHC) phenotype and collagen in 12 OSAHS patients and 8 control patients. We also distinguished the muscle isoforms I , II with ATPase staining, then counted the numbers of isoforms muscle fiber. RESULT: The mRNA expression of OSAHS group was more than control group in II A MyHC phenotype (P<0.01). The number of OSAHS group muscle fibre I isoform was less than control group with pH4. 3 ATPase staining (P<0.05). CONCLUSION Compare to control group, the enhancement happened in the mRNA expression of II A MyHC phenotype which can increase the velocity and power but de crease the enduring quality of muscle in OSAHS, and the reduce be in the I MyHC isoform of muscle fiber that can cause muscle velocity become slower and persistency become longer in OSAHS patients.
Case-Control Studies ; Female ; Humans ; Male ; Middle Aged ; Muscle Fibers, Skeletal ; metabolism ; pathology ; Myosin Heavy Chains ; metabolism ; Palate, Soft ; metabolism ; pathology ; Phenotype ; Protein Isoforms ; metabolism ; RNA, Messenger ; genetics ; Sleep Apnea, Obstructive ; metabolism ; pathology

OBJECTIVETo investigate the effects of nuclear factor kappa B (NF-kappaB) on insulin signaling in skeletal muscle cells of rat with sepsis.

METHODSSD rats were randomly divided into two groups: control group and sepsis group.Sepsis model was reproduced by cecal ligation and puncture in sepsis group. At 8, 16, 24, 48 and 72 h after operation, the gastrocnemius was harvested. Conventional HE staining was used to observe the morphology of skeletal muscle cells. IRS-1 protein and tyrosine phosphorylation of IRS-1 and Ser(307) phosphorylation of IRS-1 were detected by Western Blotting and immuno-precipitation. Activities of NF-kappaB in skeletal muscle cells were detected by electrophoretic mobility shift assay.

RESULTSTyrosine phosphorylation of IRS-1 in sepsis group was significantly lower than in control group (P < 0.01), while Ser(307) phosphorylation of IRS-1 in sepsis group was significantly higher than in control group (P < 0.01). In sepsis group, NF-kappaB activity in skeletal muscle cells was significantly higher than in control group (P < 0.01). There was significant negative correlation between activity of NF-kappaB and tyrosine phosphorylation of IRS-1 (r = 0.972, P < 0.01). There was significant positive correlation between activities of NF-kappaB and Ser(307) phosphorylation of IRS-1 (r = 0.969, P < 0.01).

CONCLUSIONSThere is no inflammatory cell infiltrate in skeletal muscle cells with sepsis. But the activity of NF-kappaB in skeletal muscle cells is obviously enhanced, and it is closely related with disorder of insulin signaling in skeletal muscle cells of rat with sepsis.

Animals ; Disease Models, Animal ; Insulin ; metabolism ; Insulin Receptor Substrate Proteins ; metabolism ; Male ; Muscle Fibers, Skeletal ; metabolism ; pathology ; NF-kappa B ; metabolism ; physiology ; Phosphorylation ; Random Allocation ; Rats ; Rats, Sprague-Dawley ; Sepsis ; metabolism ; pathology ; Signal Transduction

OBJECTIVETo examine mitochondrial DNA mutations in mitochondrial myopathy.

METHODSThree suspected cases of mitochondrial myopathy were examined by HE staining, histochemical staining methods and electron microscopy. The mutations in all 22 tRNA genes of mitochondrial genome were screened by polymerase chain reaction-single strand conformation polymorphism and DNA sequencing.

RESULTSThe three cases were diagnosed as mitochondrial myopathy. The examinations revealed that patient 1 had a homoplasmic A1627G mutation in tRNA-Val gene, and patient 2 had a heteroplasmic A1627G/A mutation in tRNA-Val gene, and patient 3 had two mutationsuone was homoplasmic T5554C mutation in tRNA-Trp gene, the other was heteroplasmic A10412C/A mutation in tRNA-Arg gene.

CONCLUSIONtRNA genes mutations of mtDNA might be one of the etiologies of mitochondrial myopathy.

Adult ; DNA Mutational Analysis ; DNA, Mitochondrial ; chemistry ; genetics ; Female ; Humans ; Male ; Microscopy, Electron, Transmission ; Mitochondrial Myopathies ; genetics ; pathology ; Muscle Fibers, Skeletal ; metabolism ; pathology ; ultrastructure ; Mutation ; Polymerase Chain Reaction ; Polymorphism, Single-Stranded Conformational ; RNA, Transfer, Val ; genetics ; Young Adult

PURPOSE: The purpose of this study was to determine the effect of dehydroepiandrosterone (DHEA) on recovery of muscle atrophy induced by Parkinson's disease. METHODS: The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 20 microg) into the left striatum using stereotaxic surgery. Rats were divided into two groups; the Parkinson's disease group with vehicle treatment (Vehicle; n=12) or DHEA treatment group (DHEA; n=22). DHEA or vehicle was administrated intraperitoneally daily at a dose of 0.34 mmol/kg for 21 days. At 22-days after DHEA treatment, soleus, plantaris, and striatum were dissected. RESULTS: The DHEA group showed significant increase (p<.01) in the number of tyrosine hydroxylase (TH) positive neurons in the lesioned side substantia nigra compared to the vehicle group. Weights and Type I fiber cross-sectional areas of the contralateral soleus of the DHEA group were significantly greater than those of the vehicle group (p=.02, p=.00). Moreover, extracellular signal-regulated kinase (ERK) phosphorylation significantly decreased in the lesioned striatum, but was recovered with DHEA and also in the contralateral soleus muscle, Akt and ERK phosphorylation recovered significantly and the expression level of myosin heavy chain also recovered by DHEA treatment. CONCLUSION: Our results suggest that DHEA treatment recovers Parkinson's disease induced contralateral soleus muscle atrophy through Akt and ERK phosphorylation.
Animals ; Corpus Striatum/drug effects/metabolism ; Dehydroepiandrosterone/*pharmacology/therapeutic use ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Male ; Muscle Fibers, Slow-Twitch/drug effects ; Muscle, Skeletal/drug effects/metabolism ; Muscular Atrophy/drug therapy/*etiology/*pathology ; Myosins/metabolism ; Neurons/drug effects/enzymology ; Oxidopamine/toxicity ; Parkinson Disease, Secondary/*chemically induced/*complications ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Sprague-Dawley ; Tyrosine 3-Monooxygenase/metabolism