〔Abstract〕 Objective To explore the pathogenesis of skeletal myopathy in patients with heart failure by observing the effects of dexmedetomidine on the proliferation and differentiation of mouse myoblast C2 C12. Methods Immunohistochemistry was used to analyze the expression characteristics of adrenergic receptors in C2 C12 cells.C2 C12 cells were divided into 6 groups: the control group and dexmedetomidine 5 concentration gradient groups(5, 10, 20, 40, 80 mmol/L). CCK-8 method was used to detect the effect of dexmedetomidine on C2 C12 cells proliferation. Differentiation medium was used to induce the differentiation of C2 C12 cells, and C2 C12 cell were dosed with single or continuous single administration. After 6 d of cell differentiation, the expression levels of myosin heavy chain(MYH), myocyte enhancer factor 2 C(MEF2 C) and myogenin(MyoG) in different groups were detected by immunofluorescence, and the number of myotubes containing different nuclei of C2 C12 cells was quantitatively analyzed.C2 C12 cells were divided into two groups: the control group and dexmedetomidine group(20 mmol/L). Then C2 C12 cells were dosed with continuous single administration and the expression levels of MYH, MEF2 C and MyoG of differentiated C2 C12 cells on the 2 nd, 4 th and 6 th day in different groups were detected by immunofluorescence. Results C2 C12 cells exhibited the characteristics of α2-adrenergic receptor expression. CCK-8 assay showed that dexmedetomidine inhibited the proliferation of C2 C12 cells in a concentration-dependent manner(P<0.05).The effect of single administration of dexmetomidine on the differentiation of C2 C12 cells was less significant than the effect of the continuous single administration of dexmetomidine, and with the increase of concentration in the continuous single administration of dexmetomidine groups, the expression levels of MYH, MEF2 C, MyoG gradually decreased, the number of C2 C12 cells differentiated into myotubes with multiple cell nuclei gradually decreased(P<0.05). On the 2 nd, 4 th and 6 th day after differentiation of C2 C12 cells, the expression levels of MYH, MEF2 C, MyoG in the 20 mmol/L group were all lower than those in the control group. Conclusion α2 adrenergic receptors exists in mouse myoblast C2 C12. Dexmetomide may inhibit the proliferation and differentiation of C2 C12 cells by binding to α2 adrenergic receptors, which is closely related to the decrease of the MEF2 C and MyoG expression levels.