Artigo de Periódico
Local inhibition of nitrergic activity in tenotomized rats accelerates muscle regeneration by increasing fiber area and decreasing central core lesions
Registro en:
1414-431X
Autor
SEABRA, Aline Damasceno
MORAES, Suellen Alessandra Soares de
BATISTA, Evander de Jesus Oliveira
GARCIA, Tarcyane Barata
SOUZA, Martha Costa de
OLIVEIRA, Karen Renata Matos
SILVA, Anderson Manoel Herculano Oliveira da
Institución
Resumen
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 No-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.