PURPOSE: This study was to determine the effect of DHEA administration before, during, and after dexamethasone treatment on body weight and TypeI,II muscle weight of rat receiving dexamethasone treatment. METHOD: Wistar rats were divided into 6 groups: control(C), dexamethasone(D), DHEA administration for 3days after dexamethasone treatment for 7days(7D+3DH), dexamethasone treatment for 7days after DHEA administration for 3days(3DH+7D), DHEA administration during dexamethasone treatment for 4days after dexamethasone treatment for 3days(3D+4DDH), DHEA administration during dexamethasone treatment for 7days(7DDH). Dexamethasone was injected by subcutaneously daily at a dose of 5mg/kg. DHEA was orally administered daily at a dose of 5mg/kg for 7 days. Soleus(TypeI) muscle, and both plantaris and gastro- cnemius(TypeII) muscles were dissected on the 7th day of experiment. RESULT: Body weight of both 3DH+7D group and 3D+4DDH group increased significantly compared with that of 7D group. Body weight of 7D+3DH group decreased significantly compared with that of 7D group, 7DDH group, 3DH+7D group and 3D+4DDH group. Muscle weight of both plantaris and gastro- cnemius tended to decrease compared with that of 7D group. Muscle weight of 7DDH group, 3D+4DDH group and 3DH+7D group increased significantly compared with that of 7D+3DH group. Muscle weight of gastrocnemius of both 3DH+7D group and 3D+4DDH group increased significantly compared with that of 7D group. CONCLUSION: Based on these results, it can be suggested that DHEA administration before and during dexamethasone treatment can increase both body weight and mass of atrophied TypeII muscle induced by dexa- methasone treatment.
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.
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.
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.
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.
The purpose of this study was to determine the effect of dehydroepiandrosterone (DHEA) on recovery of muscle atrophy induced by Parkinson's disease.
The rat model was established by direct injection of 6-hydroxydopamine (6-OHDA, 20 µg) 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.
The DHEA group showed significant increase (
Our results suggest that DHEA treatment recovers Parkinson's disease induced contralateral soleus muscle atrophy through Akt and ERK phosphorylation.