PO-235耐力训练可提高T2DM大鼠胸主动脉心肌素的表达

Derun Gao
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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. \nMethods 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 left common carotid artery intubation, blood sugar was test by enzyme chemical assay, α-SM-actin, SM-MHC , SM22α,Myocardin and KLF4 were measured through ELISA.  \nResults 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 significantly up-regulated, and the expression of α-SM-actin, SM22α and Myocardin was significantly up-regulated. \nConclusions 8 weeks of endurance training significantly increased the expression level of contractile protein in the aorta smooth muscle of diabetic rats, making the smooth muscle phenotype changed from synthetic to contractile type, which effectively inhibited the excessive proliferation and migration of smooth muscle cells.Myocardin is one of the hot spots in the study of vascular differentiation in recent years. 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摘要

目的近年来,大量实验研究表明,VSMC的增殖和迁移是AS、高血压、血管成形术后再狭窄等多种血管疾病的病理基础。VSMC的表型调控在其增殖和迁移过程中起着重要的作用。心肌素是目前为止VSMC分化的关键转录因子,能有效激活SMC的分化过程。许多研究表明,耐力训练是改善糖脂代谢的有效途径。本研究试图探讨长期外应激(耐力训练)通过继发性血管疾病对动脉平滑肌表型调节和心肌素的影响,为T2DM继发性疾病的运动治疗提供理论支持和实践依据。方法将雄性SD大鼠随机分为普通饲料组(pC)和高糖高脂饲料组(pD)。7周后,经腹腔注射小剂量链脲佐菌素。72h后非空腹血糖(NFBG)≥16.7mmol/L且伴有胰岛素抵抗者诊断为糖尿病。随后,将pC组随机分为空白对照组(C)、耐力训练组(E)、糖尿病模型组(D)、糖尿病+耐力训练组(DE)。E&DE组进行空载平台训练,每周5天,连续8周。8周后,经左颈总动脉插管测血压,酶化学法测血糖,ELISA法测定α-SM-actin、SM-MHC、SM22α、心肌素、KLF4。结果1。与C比较,D颈动脉MCP(颈动脉血压)显著升高,FBG、FINS显著降低,α-SM-actin、SM-MHC、SM22α、心肌蛋白表达显著降低,KLF4显著升高。与D组比较,E组FBG表达显著下调,FINS表达显著上调,α-SM-actin、SM22α和心肌素表达显著上调。结论8周耐力训练显著提高糖尿病大鼠主动脉平滑肌收缩蛋白表达水平,使平滑肌表型由合成型转变为收缩型,有效抑制了平滑肌细胞的过度增殖和迁移。心肌素是近年来血管分化研究的热点之一。这项研究表明,耐力训练在改善斑块形成和降低血压方面的作用可能是通过调节心肌素产生的。
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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 left common carotid artery intubation, 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 significantly up-regulated, and the expression of α-SM-actin, SM22α and Myocardin was significantly up-regulated. Conclusions 8 weeks of endurance training significantly increased the expression level of contractile protein in the aorta smooth muscle of diabetic rats, making the smooth muscle phenotype changed from synthetic to contractile type, which effectively inhibited the excessive proliferation and migration of smooth muscle cells.Myocardin is one of the hot spots in the study of vascular differentiation in recent years. This study shows that the role of endurance training in improving plaque formation and lowering blood pressure may be produced by regulating myocardin.
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