| Objective: Cardiac hypertrophy is a kind of adaptive process generatedby heart to various stimulations, which is slow but effective. The pathologicalprocess of cardiac hypertrophy includes the hypertrophy of myocardial cell,the differentiation and proliferation of fibroblast, the deposition ofextracellular matrix and the remodeling of small vessels within the myocardialwall. The manifestation of its early changes was compensatory hypertrophy,which could enhance the cardiac pump function in the short term to make theheart maintain a normal and effective circulating blood volume andconsiderable reserve capacity. This process is also known as cardiacremodeling. If this stimulation can’t be improved for a long time, however, itwill lead to cardiac decompensation hypertrophy and the decreasing of cardiacdiastolic and systolic function,inducing cardiac functional defect ultimately,which will increasing the risk of arrhythmia, heart failure and even suddendeath[1].Enkephalin which is also called B-type Natriuretic Peptide(BNP) is akind of polypeptides neurohormone separating from pig brain by Japanesehakeems Sudoh,et al~[2]. It is synthesized and secreted by myocardial cellsreactively when the blood volume increase sharply inducing the change ofventricular wall’s tension and over loading of heart ventricle’s pressure. Itplays the role of natriuretic, diuresis, relaxation of vascular, antagonism torenin-angiotensin-aldosterone system(RAAS), inhibiting the activity ofsympathetic nervous system(SNS),et al. BNP can also be used for thediagnosis of disease of cardiovascular system, the evaluation of cardiacfunction and the authentication between cardiac dyspnea and noncardiacdyspnea. In addition, the level of BNP in circulation can be used as animportant reflection for the treatment effectiveness of heart failure. It has been confirmed that the level of BNP in blood plasma would raise in the process ofmyocardial hypertrophy. Therefore, the content of BNP can be used as anindex for the degree of myocardial cell hypertrophy.The study of modern pathophysiology indicate that neuroendocrinecytokines will promote the development of cardiac remodeling significantly ifit is in a chronic and activated status which play a important role in theprogress of cardiovascular diseases. Recent studies show that adipose tissue isan active endocrine organ, secreting a variety of bioactive substance calledadipocytokines~[3,4]. These adipocytokines involve cytokine,such as tumornecrosis factor(TNF)-α and interleukin(IL)-6; chemotactic factor, such asmonocyte chemotactic protein(MCP)-1and IL-8; hormone, such as leptin,visfatin, adiponectin and resistin[5,6]. Among these, visfatin, found in2005byFukuhara et al, is a kind of cDNA fragment which is the same with the5’-UTR sequence of pre-B cell colony-enhancing factor(PBEF). This cDNAfragment is highly expressed in abdominal visceral adipose tissue in humanand mouse, that’s why it is named visfatin. Visfatin possesses an insulin-likeeffect as well as lowers blood sugar and improves peripheral insulin resistance.In addition, it is also involved in a variety of pathological processes, such asinflammatory reaction,the hyperplasia of cardiac muscle fibers,endothelialdysfunction and vascular injury. However, there is no report about what kindof impact visfatin will produce on myocardial cells and whether it will lead tomyocardial cell hypertrophy. This study was designed to investigate whetherrecombinant rat visfatin will lead to myocardial cell hypertrophy by observingthe impact of neonatal rat cardiac myocytes which were cultured in vitro withdifferent concentrations of recombinant rat visfatin or with the sameconcentration of recombinant rat visfatin at different time on the surface areaof myocardial cells, the level of BNP-mRNA in myocardial cells and BNP inculture medium.Accordingly, it can add new ideas for the pathogenesis ofdisease of cardiovascular system and provide new target for the field ofcardiovascular research.Method: We chose myocardial cells from Sprague-Dawley Rats that were newborn for2-3days in primary culture under sterile conditions andregardless of gender. The cells were cultured in serum-containing medium forthe first48hours, then in serum-free medium for another24hours, After that,we divided the cells that were in well Growth state into nine groups randomly:there were four groups according to different concentrations of recombinantrat visfatin:①control,②10ng/mLgroup,③50ng/mL group,④100ng/mLgroup; there were five groups according to different time:①c ontrol,②12hours group,③24hours group,④48hours group,⑤72hours group.Afterintervening with different concentrations of recombinant rat visfatin for24hours and with different time in100ng/mL visfatin, we used image analysissoftware to measure the surface area of myocardial cells. At the same time,real time-PCR and Elisa were used to detect the level of BNP-mRNA inmyocardial cells and BNP in culture medium in different groups.Result:1. The surface area of rat myocardial cells, the level of BNP-mRNA inmyocardial cells and BNP in culture medium all increased with theincreasing of visfatin concentration.Furthermore, they all peaked in100ng/mL group. Among the groups, the number of pairwise comparisonsshowed significant differences(P<0.05).2. The surface area of rat myocardial cells, the level of BNP-mRNA inmyocardial cells and BNP in culture medium all increased with time Within48hours under concentration of100ng/mL. Among the groups, the number ofpairwise comparisons showed significant differences(P<0.05). After48hours,they were lower than those in48hours group. However, there were nosignificant statistical difference(P>0.05).Conclusion: Visfatin could lead to myocardial cell hypertrophy. Thedegree of myocardial cell hypertrophy increased with the increasing ofvisfatin concentration. Within a certain time, the degree of myocardial cellhypertrophy aggravated with time. |
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