Objective To explore the potential mechanism of Shenqi Compound Formula（SCF

参芪复方） on skeletal muscle lesions in rats model of type 2 diabetes mellitus（T2 DM）. Methods Thirty GK rats with spontaneous T2 DM were fed with high-fat diet to develop the T2 DM rat model. After success of modeling

30 GK rats were randomly divided into model group

SCF group and rosiglitazone group

with 10 rats in each group; additionally

10 Wistar rats were given normal feed as control group. SCF group was administrated with 14.4 g/（kg·d） Shenqi Compound extract; rosiglitazone group was administrated with 0.67 mg/（kg·d） rosiglitazone suspension; model group and control group were given equal volume of normal saline; the interventions in all groups were administered once daily. After eight weeks

the pathological changes of skeletal muscle mitochondria were assessed; the protein and mRNA expressions of mitochondrial fusion protein 1（Mfn1）

mitochondrial fusion protein 2（Mfn2）

optic atrophy factor 1（Opa1）

dynamic related protein 1（Drp1）

mitochondrial fission protein 1（Fis1）

mitochondrial fission factor（Mff） in the skeletal muscle mitochondria of rats were detected. Results Compared to the control group

the model group had decreased expression of Mfn1

Mfn2 protein and mRNA

and increased expression of Drp1 protein and mRNA（P<0.05）. Compared to the model group

the SCF group had higher expression of Mfn1

Mfn2 protein and mRNA

and lower expression of Drp1 protein and mRNA（P<0.05）. There were no significant differences in the protein and mRNA expressions of Mfn1

Mfn2

Opa1

Drp1

Fis1 and Mff between the SCF group and the rosiglitazone group（P>0.05）. The pathological results showed that in model group

skeletal muscle mitochondria were swollen; the cristae structure was unclear

or flocculent degeneration and vacuolar changes were observed. In SCF group

skeletal muscle mitochondria were slightly swollen; muscle fibers were neatly arranged without atrophy. In rosiglitazone group

skeletal muscle mitochondria were swollen and degenerated; vacuoles were formulated; and the cristae was disordered and blurred. Conclusion SCF can significantly improve the early pathological changes of skeletal muscle in T2 DM rats

and its mechanism is closely related to the mitochondrial dynamics.