Data/hora: 07/06/2024 06:37:55

Provedor de dados: 	56	
País: 	Brazil	
Título: 	Local inhibition of nitrergic activity in tenotomized rats accelerates muscle regeneration by increasing fiber area and decreasing central core lesions	
Autores: 	Seabra,A.D.; Moraes,S.A.S.; Batista,E.J.O.; Garcia,T.B.; Souza,M.C.; Oliveira,K.R.M.; Herculano,A.M.	
Data: 	2017-01-01	
Ano: 	2017	
Palavras-chave: 	Nitric oxide; Muscle regeneration; Atrophy; Tendon; Tenotomy.	
Resumo: 	Muscular atrophy is a progressive degeneration characterized by muscular proteolysis, loss of mass and decrease in fiber area. Tendon rupture induces muscular atrophy due to an intrinsic functional connection. Local inhibition of nitric oxide synthase (NOS) by Nω-nitro-L-arginine methyl ester (L-NAME) accelerates tendon histological recovery and induces functional improvement. Here we evaluate the effects of such local nitrergic inhibition on the pattern of soleus muscle regeneration after tenotomy. Adult male Wistar rats (240 to 280 g) were divided into four experimental groups: control (n=4), tenotomized (n=6), vehicle (n=6), and L-NAME (n=6). Muscular atrophy was induced by calcaneal tendon rupture in rats. Changes in muscle wet weight and total protein levels were determined by the Bradford method, and muscle fiber area and central core lesion (CCL) occurrence were evaluated by histochemical assays. Compared to tenotomized (69.3±22%) and vehicle groups (68.1%±17%), L-NAME treatment induced an increase in total protein level (108.3±21%) after 21 days post-injury. A reduction in fiber areas was observed in tenotomized (56.3±1.3%) and vehicle groups (53.9±3.9%). However, L-NAME treatment caused an increase in this parameter (69.3±1.6%). Such events were preceded by a remarkable reduction in the number of fibers with CCL in L-NAME-treated animals (12±2%), but not in tenotomized (21±2.5%) and vehicle groups (19.6±2.8%). Altogether, our data reveal that inhibition of tendon NOS contributed to the attenuation of atrophy and acceleration of muscle regeneration.	
Tipo: 	Info:eu-repo/semantics/article	
Idioma: 	Inglês	
Identificador: 	http://www.scielo.br/scielo.php?script=sci_arttext&pid=S0100-879X2017000300601	
Editor: 	Associação Brasileira de Divulgação Científica	
Relação: 	10.1590/1414-431x20165556	
Formato: 	text/html	
Fonte: 	Brazilian Journal of Medical and Biological Research  v.50 n.3 2017	
Fonte: 	info:eu-repo/semantics/openAccess