PO-235 Endurance training increased the expression of myocardin in thoracic aorta of T2DM rats

Objective In recent years, a large number of experimental studies have shown that the proliferation and migration of VSMC are the pathological basis of various vascular diseases, including AS, hypertension, and restenosis after angioplasty. It’s rather remarkable that Phenotypic Modulation of VSMC plays an important role in their proliferation and migration. Myocardin is a key transcription factor for the differentiation of VSMC by far, which can effectively activate the differentiation process of SMC. Many studies have shown that endurance training is an effective way to improve glucose and lipid metabolism. This study attempted to explore the effects of long-term external stress (endurance training) on arterial smooth muscle phenotype modulation and myocardin through secondary vascular disease, in order to provide theoretical support and practical basis for sports therapy in T2DM secondary diseases. Methods Male SD rats were randomly divided into the general feed group (pC) and the high-sugar and high-fat feed group (pD). After 7 weeks, rats in pD were injected a small doses of streptozotocin through abdominal cavity. Those Non-fasting Blood Glucose (NFBG) ≥16.7mmol/L after 72h and with insulin resistance were diagnosed as diabetes. Thereafter, the pC group was randomly divided into a blank control group (C), an endurance training group (E), a diabetes model group (D), and a diabetic+endurance training group (DE). No load platform training was conducted in E&DE group, 5 days per week for 8 weeks. 8 weeks after, BP was measured through leftcommoncarotidarteryintubation, blood sugar was test by enzyme chemical assay, α-SM-actin, SM-MHC , SM22α,Myocardin and KLF4 were measured through ELISA. Results 1. Compared with C, MCP (carotid blood pressure) of D increased significantly, FBG and FINS decreased significantly, expression of α-SM-actin, SM-MHC, SM22α and Myocardin Significantly dropped, KLF4 rose significantly. Compared with D, the expression of FBG in E was significantly down-regulated, FINS was ...