## 1 Introduction  
Several factors contribute towards the apoptotic mechanisms' intricacy in skeletal muscle tissue [1, 2]. These factors include (1) variant morphological and biochemical mitochondrial pools within skeletal muscle fiber types and (2) multinucleated muscle cells. Thus, it is observed that, with regard to apoptosis, the skeletal muscle represents a distinctive tissue. Moreover, in both myoblast and myotube cells the apoptotic process in skeletal muscle was suggested to be an event of natural development and has also been observed in several diseases, like Duchenne muscular dystrophy [3], to constitute an essential feature in skeletal muscle fibers.  
Within a cell death pathway, an anti-apoptotic protein, i.e., B-cell lymphoma 2 (BCL2), functions as a critical intracellular apoptosis checkpoint, which effectively subdues apoptosis in response to a variety of stimuli (death antagonist) [4]. According to a host of studies, apoptosis was inhibited by BCL2 expression, which in skeletal muscle cells [5] also identified an early stage of myogenesis. In addition, skeletal muscle cell apoptosis could ameliorate BCL2 family expression. Moreover, according to research, BCL2 expression was suggested to be imperative for large numbers of muscle cell regeneration as well as long-term muscle progenitor cell survival [6]. In skeletal muscle apoptosis, the potential importance of BCL2 expression was also demonstrated by several studies; for example, in aging tissue, as a suggested apoptosis mechanism, an age-associated BCL2 level decrease was suspected [7]. In addition, muscle cell apoptosis has been reported by other studies, evidencing the selective targeting of a BCL2-deficient one in differentiating murine myotubes [8]. Previous studies demonstrated adenosine and adenosine analogue to have a regulatory effect on apoptosis of several types of cells, for instance, human thymocytes, rat brain astrocytes, and lymphoid cells. This was evident in two independent pathways, namely, adenosine transport or/and extracellular receptor subtype activity modulations [9; 10; 11; 12].  
It was observed that the adenosine receptors, in fact, present the possibility of serving as potential cytoprotective receptors, and thus notably warrant supplementary research, particularly in the context of ameliorating skeletal muscle injury [13]. Moreover, a specific dearth in research was evident in the adenosine receptor effects in myotubes culture [14; 15]. Correspondingly, adenosine A2A receptors can be considered as new cytoprotective receptors [16], albeit warranting further investigation for skeletal muscle injury amelioration.  
However, the apoptosis impact on degradation of skeletal muscle is still ambiguous; thus, it was intriguing to study, in skeletal muscle cells, if it was possible for adenosine or adenosine analogue or related ligands to modulate anti-apoptotic (BCL2) gene expression [6]. This further presented the probability of muscle cell apoptosis inhibition, and a consequent contribution to the protection of skeletal muscle, cell regeneration or survival [8].  
The purpose of this investigation was to test the hypothesis that CG21680, NECA and/or PSB 603 treatment would significantly modulate BCL2 gene expression in rat skeletal muscle.