Effect of Buyang Huanwutang on Skeletal Muscle Injuries in Mouse Model of Type 2 Diabetes Mellitus / 中国实验方剂学杂志

ABSTRACT

ObjectiveTo study the effects of Buyang Huanwutang on the skeletal muscle injuries in type 2 diabetes mellitus from mitochondrial transport， glucose metabolism， oxidative stress， and inflammation. MethodA total of 60 SPF-grade male C57BL/6J mice were selected in this study. The mouse model of type 2 diabetes mellitus was established with a high-fat diet combined with intraperitoneal injection of streptozotocin. The mice were assigned by the random number table method into blank control， model， high-， medium-， and low-dose （86.5， 43.2， 21.6 g·kg-1， respectively） Buyang Huanwutang， and metformin （150 mg·kg-1） groups， 10 mice in each group. During the experiment period， blood glucose and other indicators of mice were measured regularly. At the end of the experiment， skeletal muscle samples were collected and frozen in 4% paraformaldehyde and -80 ℃， respectively. Blood samples were sent for examination. The skeletal muscle was stained with hematoxylin-eosin. The levels of inflammation indicators and reactive oxygen species （ROS） were determined by enzyme-linked immunosorbent assay. The expression of mitochondrial proteins was determined by Western blot and immunohistochemistry. ResultCompared with the blank control group， the model group showcased increased fasting blood glucose， water intake， and food intake （P<0.01） and decreased body weight （P<0.01）. Compared with the model group， metformin and Buyang Huanwutang reduced the fasting blood glucose， water intake， and food intake （P<0.05， P<0.01） and increased the body weight （P<0.01）. Compared with the blank control group， the model group showed rising levels of tumor necrosis factor-alpha （TNF-α）， interleukin-6 （IL-6）， and ROS （P<0.01）， which were decreased by metformin and Buyang Huanwutang （P<0.05， P<0.01）. The skeletal muscle fibers in the model group were generally atrophic and thin， which suggested atrophy and morphological changes of the skeletal muscle， while metformin and Buyang Huanwutang alleviated the pathological changes of the skeletal muscle and restored the morphology of fiber bundles. Compared with the blank control group， the modeling down-regulated the expression of the mitofusin2 （Mfn2） （P<0.01）， which was up-regulated by metformin and Buyang Huanwutang （P<0.05， P<0.01）. Compared with the blank control group， the modeling up-regulated the expression of the dynamin-related protein （Drp1） （P<0.01）， which were down-regulated by metformin and Buyang Huanwutang （P<0.01）. ConclusionBuyang Huanwutang can improve the body weight and attenuate the pathological changes of the skeletal muscle， reduce fasting blood glucose， food intake， and water intake， lower the levels of TNF-α， IL-6， and ROS， down-regulate the expression of Drp1， and up-regulate the expression of Mfn2 in the mouse model of type 2 diabetes mellitus.