| Objective: Adipose tissue is a kind of traditional energy storageorganization. As further research, the function of adipose tissue get moreunderstanding. Adipose tissue can secrete a variety of factors. Currently, thereare more than30kinds of adipocytokines, such as adiponectin, ASP, TNF-α,visfatin, IL-6, IL-8, resistin, leptin, omentin, plasminogen-activator inhibitortype1, RBP4and others. These factors not only can adjust the body’s energymetabolism and neuroendocrine function, but can participate in the body’simmune and inflammatory reaction.A lot of adipocytokines involved in incidence of cardioascular diseasedevelopment. Visfatin mainly come from visceral fat cells. Visfatin is highlyexpressed in the rich content of lipid macrophages and acute coronary lesions.Macrophages involved in inflammation, the formation of atherosclerosisrelated with inflammation, hypoxia, unstable plaques rupture and endothelialdysfunction. As a promote inflammation factor, visfatin involved in theformation of atherosclerosis. Research shows that visfatin maybe induce theformation of the foam cells and promote the formation of blood essel plaques,which causes atherosclerosis. Visfatin can promote the maturity of vascularsmooth muscle cells and cause the reshaping of blood vessels. Visfatin has therole of para-insulin, but don’t lower the insulin level. Plasmatic visfatin levelrising related with the process of heart failure, myocardial cell hypertrophyand myocardial fibrosis. That has opened up a new direction for theprevention and treatment of cardiovascular disease.Angiotensin II is the main active substance of RAAS. It can enhance thesympathetic nervous activity, promote vasoconstriction, higher blood pressure,enhance myocardial-contractive-power, speed up heart rate, and then cardiomyocyte hypertrophy formed. Angiotensin II can stimulate fibroblasts,lead to high expression of connective tissue growth factor. As a result,myocardial fibrosis formed. Angiotensin II should combine with specificreceptor （AT1AT2） to play a role on the cell membrane. AT1widedistribution, it can promote proliferation of endothelial cell and vascularsmooth muscle cell, and can promote the myocardial fibrosis andcardiomyocyte hypertrophy. The quantity of AT2in the adult body issignificantly less than embryonic organization. In the condition of stress in thebody, such as myocardial infarction, wound healing, vascular intima damageand heart failure process, the expression of AT2has increased. Studies haveconfirmed that the expression of visfatin closely related with the mediating ofAT1receptor. AT1receptor mainly has three channels, SP600125, U0126andAG490, which are the specific blocking agents of the three channelsrespectively. Previous trials confirmed that myocardial cells can expressvisfatin. Myocardial cells express the highest level of visfatin whenangiotensin II concentration is10-6mmol/l for24hours. In this experimentalstudy, we observe the relationship of the expression of visfatin with AT1receptor channels in cardiocytes.Method: Primary culture the cardiomyocytes from the hearts of2-3days’neonatal Sprague-Dawley （SD） rats aseptically, regardless of sex. After48hours’ culture with serum and24hours’ culture without serum, cells in goodconditions are selected and put into8groups randomly.①controlgroup,②10-6mol/LAngⅡgroup,③SP600125group,④U0126group,⑤AG490group,⑥10-6mol/L AngⅡ+SP600125group,⑦10-6mol/L AngⅡ+U0126group,⑧10-6mol/L AngⅡ+AG490group. Visfatin mRNA and proteinexpression in cardiomyocytes treated with Ang II10-6mol/L for24hours in thepresence of AG490, U0126or SP600125. Then detect the expression ofvisfatin-mRNA and visfatin-protein with RT-PCR and ELISA.Results:1Culture the cardiomyocytes from the hearts of2-3days’ neonatalSprague-Dawley （SD） rats successfully. 2The expression of visfatin-mRNA and protein are increased in the groupswith angiotensin II participation.3There are no difference between the SP600125group, AG490group, U0126group and control group in expression of visfatin-mRNA and protein.4The expression of visfatin-mRNA and protein are decreased in10-6mol/LAngⅡ+SP600125group,10-6mol/L AngⅡ+U0126group and10-6mol/LAngⅡ+AG490group compared with AngⅡ group.5The expression of visfatin-mRNA and protein is decreased in10-6mol/LAngⅡ+AG490group compared with10-6mol/L AngⅡ+SP600125group and10-6mol/L AngⅡ+U0126group.6The expression of visfatin-mRNA and protein has no obvious differencebetween10-6mol/L AngⅡ+SP600125group and10-6mol/L AngⅡ+U0126group.Conclusion: In cardiomyocytes, angiotensin Ⅱ upregulate theexpression of visfatin by JAK/STAT. |
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