PURPOSE: The purpose of this study was to determine the effect of DHEA on hindlimb muscles(soleus, plantaris and gastrocnemius) in a focal brain ischemia model rat. METHOD: Twenty-seven male Sprague-Dawley rats were randomly divided into three groups: CINS(cerebral ischemia + normal saline), CIDH(cerebral ischemia + DHEA), or SHNS(sham + normal saline). Both the CINS and CIDH groups underwent a transient right middle cerebral artery occlusion operation. In the SHNS group, a sham operation was done. 0.34mmol/kg DHEA was administered daily by an intraperitoneal injection for 7days. RESULT: The muscle weight, muscle fiber cross-sectional area of the Type I muscle fiber of soleus and Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of gastrocnemius, and muscle strength in the CINS group decreased compared with the SHNS group. The muscle weight, muscle fiber cross-sectional area of the Type II muscle fiber of plantaris and gastrocnemius, myofibrillar protein content of soleus, and muscle strength in the CIDH group increased compared with the CINS group. CONCLUSION: It was identified that muscle atrophy could be induced during 7 days after a cerebral infarction, and DHEA administration during the early stages of a cerebral infarction might attenuate muscle atrophy.
Animals ; Brain Ischemia/*pathology ; Dehydroepiandrosterone/*pharmacology ; Hindlimb ; Male ; Muscle, Skeletal/*drug effects/pathology ; Muscular Atrophy/chemically induced ; Rats ; Rats, Sprague-Dawley

PURPOSE: The purpose of this study was to determine the effect of Dehydroepiandrosterone (DHEA) administration alone or exercise combined with DHEA before steroid treatment on rat hindlimb muscles. METHODS: Male Sprague-Dawley rats were assigned to one of three groups: a steroid group (S, n=10) that had no treatment for 7 days before steroid treatment; a DHEA-steroid group (DS, n=8) that had 0.34 mmol/kg/day DHEA injection once a day for 7 days before steroid treatment and an exercise?steroid group (EDS, n=9) that ran on the treadmill combined with 0.34 mmol/kg/day DHEA injection for 7 days before steroid treatment. At 15 days all rats were anesthetized and soleus, plantaris and gastrocnemius muscles were dissected. Body weight, food intake, muscle weight, myofibillar protein content and cross-sectional area of the dissected muscles were determined. RESULTS: The DS group showed significant increases (p<.05) as compared to the steroid group in body weight, and muscle weight of gastrocnemius muscles. The EDS group showed significant increases (p<.05) as compared to the S group in body weight, muscle weight, myofibrillar protein content, and Type II fiber cross-sectional area of soleus, plantaris and gastrocnemius muscles. CONCLUSION: Exercise combined with DHEA administration before steroid treatment prevents steroid induced muscle atrophy, with exercise combined with DHEA administration being more effective than DHEA administration alone in preventing muscle atrophy.
Animals ; Body Weight ; Dehydroepiandrosterone/*administration & dosage ; Hindlimb ; Male ; Muscle Contraction/drug effects ; Muscle, Skeletal/*drug effects/pathology ; Muscular Atrophy/chemically induced/*prevention & control ; *Physical Conditioning, Animal ; Rats ; Rats, Sprague-Dawley ; Steroids/*toxicity

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

PURPOSE: The purpose of this study was to examine the effects of Cu/Zn SOD on reduction of hindlimb muscular atrophy induced by cisplatin in rats. METHODS: Forty-two rats were assigned to three groups; control group, Cisplatin (CDDP) group and cisplatin with Cu/Zn SOD (CDDP-SOD) group. At day 35 hindlimb muscles were dissected. Food intake, activity, withdrawal threshold, muscle weight, and Type I, II fiber cross-sectional area (CSA) of dissected muscles were measured. Relative SOD activity and expression of MHC and phosphorylated Akt, ERK were measured after dissection. RESULTS: Muscle weight and Type I, II fiber CSA of hindlimb muscles in the CDDP group were significantly less than the control group. Muscle weight and Type I, II fiber CSA of hindlimb muscles, food intake, activity, and withdrawal thresholds of the CDDP-SOD group were significantly greater than the CDDP group. There were no significant differences in relative SOD activities of hindlimb muscles between the CDDP-SOD and CDDP groups. MHC expression and phosphorylated Akt, ERK of hindlimb muscles in the CDDP-SOD group were significantly greater than the CDDP group. CONCLUSION: Cu/Zn SOD attenuates hindlimb muscular atrophy induced by cisplatin through increased food intake and activity. Increment of phosphorylated Akt, ERK may relate to attenuation of hindlimb muscular atrophy.
Animals ; Body Weight/drug effects ; Cisplatin/*toxicity ; Disease Models, Animal ; Extracellular Signal-Regulated MAP Kinases/metabolism ; Hindlimb ; Male ; Muscle, Skeletal/*drug effects/enzymology/metabolism ; Muscular Atrophy/*chemically induced/metabolism/pathology ; Phosphorylation ; Proto-Oncogene Proteins c-akt/metabolism ; Rats ; Rats, Sprague-Dawley ; Recombinant Proteins/biosynthesis/genetics/pharmacology ; Superoxide Dismutase/genetics/metabolism/pharmacology ; Superoxides/metabolism