Recently apoptotic cell death has been reported in differentiated skeletal muscle, where apoptosis was generally assumed not to occur. To investigate whether apoptosis may contribute to the steroid-induced myopathy, rats treated with triamcinolone acetonide (TA) for 9 days were sacrificed for detecting apoptosis by in situ end labeling (ISEL) and electron microscopy in the soleus muscles. Immunohistochemical stainings of Fas antigen and p53 protein were performed to examine whether apoptosis-related proteins were present in the myopathy. Muscle fiber necrosis and apoptotic myonuclei appeared in the soleus muscles following administration of TA, while control muscles showed no evidences for apoptosis. Fas antigen was not detected in control muscles, but expressed in the soleus muscles of steroid-induced myopathy. Some of the Fas antigen-expressing muscle fibers were positive for ISEL. p53 protein was not detected in any muscle fibers. These findings indicate that TA can induce apoptosis in differentiated skeletal muscles, and Fas antigen might be partly related to apoptotic muscle death in steroid-induced myopathy.
Animal ; Antigens, CD95/analysis ; *Apoptosis ; Female ; Immunohistochemistry ; Microscopy, Electron ; Muscle, Skeletal/*pathology/ultrastructure ; Muscular Diseases/chemically induced/*pathology ; Protein p53/analysis ; Rats ; Rats, Sprague-Dawley ; Triamcinolone Acetonide/*toxicity

PURPOSE: We investigated whether oxygen-induced retinopathy (OIR) results in changes in the protein expression of neuronal and inducible nitric oxide synthases (nNOS and iNOS, respectively) in rat model of OIR. In addition, we evaluated whether treatment of rats with triamcinolone acetonide (TA) prevents this response. METHODS: To promote OIR, Sprague-Dawley rats were exposed to hyperoxia from postnatal day 2 (P2) to P14. They were then returned to normoxia after P15. TA was injected into the right vitreous of P15 rats, while saline was injected into the left vitreous. At P18 the expression of nNOS and iNOS was determined using Western blotting and immunostaining techniques in retinas obtained from control rats. RESULTS: In P18 OIR rats, the abundance of nNOS and iNOS protein was significantly increased compared with controls. These increases were not observed in the retinas of rats treated with TA. The change in expression of nNOS and iNOS were specific to parvalbumin and glial fibrillary acidic protein-positive cells. Treatment with TA prevented the increased expression of nNOS and iNOS in all samples. CONCLUSIONS: Hypoxia upregulates expression of nNOS and iNOS in OIR rat retinas, which is can be prevented by treatment with TA.
Animals ; Animals, Newborn ; Anoxia/metabolism/pathology/*prevention & control ; Blotting, Western ; Disease Models, Animal ; Female ; Glucocorticoids/pharmacology ; Immunohistochemistry ; Neurons/metabolism ; Nitric Oxide Synthase Type II/*biosynthesis ; Oxygen/toxicity ; Pregnancy ; *Pregnancy, Animal ; Rats ; Rats, Sprague-Dawley ; Retina/*metabolism/pathology ; Retinal Diseases/chemically induced/pathology/*prevention & control ; Triamcinolone Acetonide/*pharmacology