Effect Of Visfatin Gene Transfer On Cardiac Hypertrophy Induced By AngⅡ In Mice

Objectives:In this study,we observed the morphology of cardiac myocytes and the expression of BNP and β-MHC in visfatin tansgenic mice induced by angiotensin Ⅱ(AngII),the aim was to investigate the role of visfatin in AngII-induced cardiac hypertrophy.Methods: Sixteen male C57BL/6 mice,8 weeks old and 20-25 g,were randomly divided into wild control group and wild AngII group.Sixteen male visfatin transgenic mice,8 weeks old 20-25 g were randomly divided into transgenic control group and transgenic AngII group.All mice were implanted with a hypodermic pump.AngII was continuously pumped at a rate of 1.3 mg/kg/day at a concentration of 5 mg/ml in the two AngII groups,while saline of equal volume was continuously pumped at the same speed in the two control groups.After 4 weeks,the mice were weighed and the mice were sacrificed by cervical dislocation.Quickly open the chest and take out the heart.The heart was removed by rapid thoracotomy.After washing 2-3 times with normal saline at 4 ℃,the heart was cut,the whole heart weight was weighed,and calculate the heart mass index(HMI).Cut the upper and lower segments of the mouse ventricle,total RNA was extracted from the upper part after quick freezing with liquid nitrogen,and the expression levels of BNP and β-MHC were detected by RT-PCR.The lower segment was fixed with formalin and sectioned.The cross-sectional area of myocardial cells was measured after HE staining.Measurement data expressed as mean ± standard deviation((?)± s),independent sample t test was used to compare the differences between groups,with P<0.05 as the statistical significance.Results: 1 The effect of visfatin gene transfer on HMI in AngII-induced cardiac hypertrophy mice:There was no significant difference in HMI between the transgenic control group and the wild control group [(4.27 +0.17)vs.(4.16 +0.15)mg/g,P>0.05].The HMI of wild AngII group was higher than that of wild control group [(5.11+0.23)mg/g vs.(4.16+0.15)mg/g,P<0.01].HMI in AngII group was higher than that in control group [(5.51 +0.18)vs.(4.27 +0.17)mg/g,P<0.01].The HMI of transgenic AngII group was higher than that of wild AngII group [(5.51+0.18)vs.(5.11+0.23)mg/g,P<0.05].2 The effect of visfatin gene transfer on cross-sectional area of myocardial in Ang II-induced cardiac hypertrophy mice:There was no significant difference in the cross-sectional area of myocardial cells between the transgenic control group and the wild control group [(201.42 +31.673)vs.(197.34±28.317)um2,P>0.05].The cross-sectional area of myocardial cells in wild AngII group was larger than that in wild control group [(427.62±76.075)vs(197.34±28.317)um2,P<0.01].The cross-sectional area of myocardial cells in AngII group was larger than that in control group [(544.43±81.984)vs(201.42 +31.673)um2,P < 0.01].The cross-sectional area of myocardial cells in transgenic Ang II group was larger than that in wild AngII group [(544.43±81.984)vs(427.62±76.075)um2,P < 0.01].3 The effect of visfatin gene transfer on mRNA expression level in AngII-induced cardiac hypertrophy mice:(1)There was no significant difference in the expression of β-MHC in myocardial cells between the transgenic control group and the wild control group(P>0.05).The expression level of β-MHC in myocardial cells of two AngII groups was higher than that of the corresponding control group(all P<0.01).The expression level of β-MHC in myocardial cells of transgenic AngII group was higher than that of wild AngII group(P <0.05).(2)There was no significant difference in the expression of BNP in myocardial cells between the transgenic control group and the wild control group(P>0.05).The expression level of BNP in myocardial cells of two AngII groups was higher than that of the corresponding control group(allP<0.01).The expression level of BNP in myocardial cells of transgenic AngII group was higher than that of wild AngII group(P <0.05).Conclusion:1 The simple transfer of visfatin gene does not promote cardiac hypertrophy.2 The transfer of visfatin gene can change the process of cardiac hypertrophy induced by angiotensin Ⅱ,and significantly increase the degree of cardiac hypertrophy induced by angiotensin Ⅱ.3 The expression of BNP increased significantly in hypertrophic myocardium induced by angiotensin Ⅱ.