Relation between microcurrent therapy and satellite cells in the regeneration of induced skeletal muscle injury in rat

Severe injuries in skeletal muscle result in muscle weakness, which delays recovery and contributes to progressive decline in muscle function. Microcurrent therapy is a novel treatment method used in soft-tissue injury and tissue regeneration therapy. The regenerative capacity of skeletal muscle tissue resides in satellite cells, the quiescent adult stem cells. The present work aimed at investigating the possible relation between microcurrent therapy and satellite cells in regeneration of induced skeletal muscle injury in albino rats. Twenty-four male albino rats were divided into 2 groups: Control group and experimental group [II]: rats were subjected to gastrocnemius-soleus muscle injury [subgroup IIa], they were subdivided into subgroups IIa1 and IIa2 sacrificed 1 and 3 weeks after injury respectively. Subgroup IIb: Rats were subjected to muscle injury and micro-current electric stimulator, was applied for 20 minutes for three sessions per week. The animals were subdivided into subgroups IIb1 and IIb2 sacrificed 1 and 3 weeks following the day of injury. Muscle sections were stained with hematoxylin and eosin, alpha smooth muscle actin [alpha-SMA] and CD34 immunostaining. Morphometric studies and statistical analysis were performed. Atypical fibers were widely separated by connective tissue cells and revealed partial loss of striations in subgroup IIa. Some fibers recruited strong acidophilic sarcoplasm with focal vacuolations in subgroup IIa1. In subgroup IIb1, some typical fibers, some centrally located nuclei, and a few deeply acidophilic fibers were found. Striations were found in some areas of the sarcoplasm. In subgroup IIb2 striations were found in most areas of the sarcoplasm. A significant decrease in the mean area of atypical fibers, a significant increase in the mean area% of alpha-smooth muscle actin-positive cells, and a significant increase in the mean area% of CD34-positive cells were found in subgroup IIb compared with subgroup IIa. A definite therapeutic effect of the microcurrent was found on induced skeletal muscle injury, which was time dependent. This effect was proved to be related to satellite cell activation

Effect of thyroid hormone on contractility and sarco/endoplasmic Reticulum Ca[2+] ATPase -1 [SERCA1] expression in adult rats; role in thermogenesis

Thyroid hormone is one of the main factors that determine skeletal muscle contractile properties and the slow-twitch vs. fast twitch muscle fiber phenotype. Sarcoplasmic reticulum Ca[2+] ATPase is one of the principal regulators of Ca[2+] homeostasis in the skeletal muscle cells. It has been previously shown that modification of thyroid hormone levels has a profound impact on cardiac function, predominantly through a direct regulation of the sarcoplasmic reticulum protein levels. The present study aimed to investigate the effects of thyroid hormone treatment for 4 weeks on slow twitch soleus muscle of rats via recording twitch tension, time to peak tension, and half relaxation time and determination of soleus muscle SERCA1 expression. 24 male rats of local strain were randomly divided into 2 groups [n=12], control euthyroid group and hyperthyroid group in which hyperthyroidism was induced by intra peritoneal [i.p] injection of L-troxin 200microg/kg B.W./day, for 4 weeks. The in-situ isometric measures were done for soleus muscle and twitch tension [TT], [expressed as screen units], time to peak tension [TPT], and half relaxation time, 1/2 Rt [expressed in milliseconds] were recorded. SERCA1 protein expression in rat soleus muscle was measured. Thyroid hormone treatment significantly reduced time to peak tension and half relaxation time and increased twitch tension. These contractile changes were accompanied with significant increase in expression of SERCA1 in soleus muscle of rats. Thyroid hormone stimulates the expression of SERCA1 in slow soleus muscle in rats, thereby speeding-up the contraction-relaxation cycle and this increases energy expenditure and these effects of thyroid hormone participate at least in part to thermogenic action of thyroid hormone