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Effect of acute ankle inflammation on histological features, gene expression and levels of creatine kinase and antioxidant enzymes in the soleus and anterior tibialis muscles of diabetic rats


Skeletal muscle is one of the most adaptable tissues in the body and certain chronic diseases of great relevance to public health, such as diabetes mellitus, cause significant muscle atrophy. When a joint injury occurs, the muscle functionally related to that joint undergoes a process of muscle atrophy, in which its strength and cross-sectional area decrease and there are proprioceptive and functional changes. The study of this process is important, since in a case of joint inflammation, physiotherapy is directed primarily at the joint disease, but the muscle should not be forgotten as an object of intervention. Experimental studies that help to elucidate the relationship between joint inflammation and histological changes and alterations of gene expression in the muscle of diabetic animals have not been reported. Other important parameters that should be studied are the activities of creatine kinase and antioxidant enzymes, since their intracellular levels should be involved in the process of tissue repair. The aim of this project is to study the effect of acute inflammation of the ankle on the soleus and anterior tibialis muscles, investigating the presence of histological changes and altered gene expression and the activity of creatine kinase, catalase, superoxide dismutase and glutathione peroxidase in these muscles, in normal and diabetic rats, with and without insulin treatment. (AU)

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(References retrieved automatically from Web of Science and SciELO through information on FAPESP grants and their corresponding numbers as mentioned in the publications by the authors)
PINHEIRO-DARDIS, CLARA MARIA; GUTIERRES, VANIA ORTEGA; ASSIS, RENATA PIRES; PEVIANI, SABRINA MESSA; DELFINO, GABRIEL BORGES; QUAGLIOTTI DURIGAN, JOAO LUIZ; SALVINI, TANIA DE FATIMA; BAVIERA, AMANDA MARTINS; BRUNETTI, IGUATEMY LOURENCO. Insulin treatment reverses the increase in atrogin-1 expression in atrophied skeletal muscles of diabetic rats with acute joint inflammation. THERAPEUTICS AND CLINICAL RISK MANAGEMENT, v. 14, p. 275-286, . (10/00892-0)

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