AIMTo study the effect of radix-astragali compound(RC) on muscle atrophy in tail-suspended rats. Muscle weight, fiber type distribution, cross-sectional area (CSA), and activity of myosin adenosine triphosphatase (ATPase) in rat soleus muscle were investigated.

METHODSThe tail-suspended rats were subjected to a 14 days simulated weightlessness, during which period, RC or saltwater was given via intragastric instillation during tail suspension. The changes of soleus muscle weight were scaled by muscle-to-body weight ratio. The activities of myosin ATPase of muscle fibers were detected by method of Ca(2+) -ATPase.

RESULTSAfter a 14 days tail suspension it was found: in rats treated with RC, soleus muscle-to-body weight ratio rose by 33.33% (P < 0.01), both CSA of type I and II fiber drastically enhanced by(143.03%, P < 0.01; 83.25%, P < 0.01), the percentage of type I fiber significantly declined compared to the untreated rats.

CONCLUSIONRC is able to effectively prevent muscle atrophy caused by tail suspension and restrain the increase in the myosin ATPase activities caused by simulated weightlessness.

Animals ; Drugs, Chinese Herbal ; pharmacology ; Hindlimb Suspension ; Male ; Muscle Fibers, Skeletal ; enzymology ; Muscle, Skeletal ; drug effects ; enzymology ; Muscular Atrophy ; prevention & control ; Myosins ; metabolism ; Rats ; Rats, Sprague-Dawley ; Weightlessness Simulation ; methods

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

trans-Resveratrol (t-RVT), a naturally occurring polyphenol found in Polygonum cuspidatum, grape, and red wine, has been reported to have anti- inflammatory, cardioprotective, and cancer chemopreventive properties. However antidiabetic effect of t-RVT has not yet been reported. In this study, we show that t-RVT increases glucose uptake in C2C12 myotubes by activating AMP-activated protein kinase (AMPK), uncovering an antidiabetic potential of t-RVT for the first time. AMPK plays a central role in the regulation of glucose and lipid metabolism, and hence it is considered a novel therapeutic target for metabolic syndrome such as type 2 diabetes. t-RVT significantly induced glucose uptake in C2C12 cells, via AMPK activation, but not a phosphatidylinositol-3 kinase (PI-3 kinase) signal pathway. The induced glucose uptake was attenuated by pretreatment with a pharmacological inhibitor for AMPK, indicating that the effect of t-RVT primarily depends on AMPK activation. However, in the presence of insulin, t-RVT also potentiated the effect of insulin on glucose uptake via AMPK activation, which led to further activation of PI-3 kinase/Akt signal pathway.
1-Phosphatidylinositol 3-Kinase/metabolism ; AMP-Activated Protein Kinases ; Animals ; Biological Transport/drug effects ; Cell Line ; Enzyme Activation/drug effects ; Glucose/*metabolism ; Insulin/metabolism ; Mice ; Models, Biological ; Multienzyme Complexes/*metabolism ; Muscle Fibers, Skeletal/*drug effects/enzymology/metabolism ; Protein-Serine-Threonine Kinases/*metabolism ; Proto-Oncogene Proteins c-akt/metabolism ; Stilbenes/*pharmacology