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Objective: The conventional wisdom is that adipose tissue is a storage organ of energy. In recent years, the adipose tissue as an endocrine organ has become the academic consensus secrete numerous adipocytokines, including tumor necrosis factor-α (TNF-α), interleukin -6 (IL-6), interleukin-8 (IL-8 ), blood plasminogen activator inhibitor (PAI-1), leptin (of leptin), adiponectin (adiponectin), resistance to hormone (resistin), visfatin (visfatin). The adipocytokines in maintaining normal body energy metabolism, inflammation, vascular endothelial cells and smooth muscle cell function, stress has an important influence in many ways. Obesity with the accumulation of fat and an increase of the size of fat cells, fat cells factor secretion disorders, and ultimately lead to a range of obesity-related atherosclerosis, hypertension, diabetes, metabolic syndrome and other diseases. Fukuhara [1] using differential display method body subcutaneous fat and visceral fat PCR products were screened, found that a high visceral fat-specific mRNA expression. The sequencing results showed that the cDNA fragment with pre-B cell clones enhancement factor (Pre-B-coloning the enhance factor, PBEF) gene 5 'UTR sequence identical visfatin is also known as PBEF. Visfatin as a newly discovered adipocytokine, which is mainly derived from the visceral adipose tissue, has contemplated insulin activity, can lower blood sugar. Visfatin may directly promote vascular inflammation bridges Contact metabolic disorders including atherosclerosis and coronary atherosclerotic disease artery atherosclerotic disease thrombosis in the context of chronic inflammation. Visfatin in visceral fat cells. At the same time, were expressed in skeletal muscle, liver, bone marrow stromal cells, lymphocytes [5]. Whether the expression of visfatin cardiac myocytes, angiotensin II stimulation of myocardial cells visfatin expression since no reports of what role. Examined the effects of different concentrations of angiotensin II, different time on cultured neonatal rat cardiomyocytes visfatin expression to explore the expression of the angiotensin II stimulation of myocardial cells visfatin to cardiovascular disease The pathogenesis of new content, new ideas, provide a new target for clinical treatment. : Sterile test conditions, gender-neutral extraction nascent 2-3 days of Sprague-Dawley (SD) rats myocardial cells in primary culture, serum-containing culture 48 hours, 24 hours after the withdrawal of serum-free culture, select a good state of growth The cells were divided into 10 groups. Different concentrations of angiotensin II five groups: ① angiotensin II 10 -8 sup> mol / L group, ② angiotensin II 10 -7 sup> mol / L group, ③ angiotensin Su Ⅱ 10 -6 sup> mol / L group, of ④ angiotensin II 10 -5 sup> mol / L group, ⑤ control group. Five different time the ① 6h group ② 12h group, ③ 24h group, ④ 48h group, the ⑤ control group. Intervention in the 48 hours to different concentrations of angiotensin II and angiotensin Ⅱ (10 -6 sup> mol / L) at different time to GAPDH as an internal control, RT-PCR and western-blot detect myocardial cells visfatin mRNA and protein expression levels. Results: 1 SD rat myocardial cells were successfully cultured in vitro. 2 with the angiotensin II concentration increased, the increase in myocardial cell viability, and at a concentration of 10 -6 sup> mol / L with angiotensin II concentration further increase myocardial cell viability decreased. 3 with angiotensin II concentration increased, myocardial cells Visfatin-mRNA and protein expression was significantly increased. 4 angiotensin Ⅱ stimulated myocardial cell viability in a time-dependent manner, and reached a peak of 12 hours, and 24 hours after myocardial cell viability decreased. The 5 myocardial cells the angiotensin Ⅱ within 24h, the extension of the time with the role of visfatin the the visfatin-mRNA and protein expression increased significantly; 48h, visfatin the visfatin-mRNA and protein expression with respect to the role of decreased 24h . Conclusion: The myocardial cells can express visfatin. Angiotensin II promotes the increase in the level of visfatin expression in vitro in cultured myocardial cells. With the angiotensin II concentration increased, the expression level of the myocardial cells visfatin has increased gradually. In the the angiotensin Ⅱ role 24h, the expression level of the myocardial cells visfatin significantly increased with time.
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