| ObjectiveTo set up the module of heart failure with preserved left ventricular ejection fraction HFpEF on rats.To explore the role of dietary zinc concentration changes in HFpEF.MethodsA group of 6-week-old Dahl salt-sensitive rat(DSS rat)was used to establish a rat model of heart failure with preserved left ventricular ejection fraction(HFpEF).DSS rats were randomly divided into 4 experimental groups and 1 control group,which were high salt and high zinc group,high salt high zinc group,high salt normal zinc group,high salt low zinc group and normal salt normal zinc group(Control group).The total content of sodium chloride in the high salt group was 8%,and the total content of sodium chloride in the control group was 0.3%.The total zinc content in the extremely high zinc group was 270 mg/kg,the total zinc content in the high zinc group was 90 mg/kg,the total zinc content in the normal zinc group was 30mg/kg,and the total zinc content in the low zinc group was 10 mg/kg.The feeding conditions of each group and the other components except zinc ions and sodium chloride in the feed were the same.Body weight,non-invasive blood pressure,and heart rate were monitored every two weeks for each group of animals,and echocardiography was performed at 7 weeks and 20 weeks of age.After feeding to 20 weeks of age,blood,myocardial and wet lung samples were obtained from rats.The BNP content in the model blood was determined by enzyme-linked immunosorbent assay(ELISA).The expression of BNP mRNA in myocardial tissue was determined by Real-time Quantitative Polymerase Chain Reaction(qPCR).The expression of BNP protein in myocardial tissue was determined by Western Blot.Wet lung specimens were dried and weighed again to calculate wet lung/dry lung results.The above data was used to verify the success of the modeling,and the influence of changes in dietary zinc concentration on HFpEF was explored by statistically comparing the differences in modeling data between groups.ResultsWhen fed to 20 weeks of age,rats in the high-salt diet group experienced weight loss,loss of appetite,gray hair,and decreased activity.The systolic and diastolic blood pressure levels in the high-salt diet group were significantly higher than those in the control group,and the difference was statistically significant(p<0.05),but there was no significant difference in blood pressure levels between the groups treated with different zinc concentrations.There was no significant difference in heart rate between the groups.The high-salt normal zinc group had higher body weight,high zinc,high salt and low zinc,and the control group was relieved,the difference was statistically significant(p<0.05).The high-salt and high-zinc group had higher body weight and lower zinc group and the control group,and the difference was statistically significant(p<0.05).The high-salt-high-zinc group had higher body weight and low-zinc group and the control group,but the difference was not statistically significant.Echocardiographic data indicated that the E/A ratio decreased,the end-diastolic interventricular septal thickness(IVSd)thickened,the end-diastolic left ventricular diameter(LVDd)decreased,and the end-diastolic left ventricle decreased in the high-salt diet group at 20 weeks of age.Wall thickness(LVPWd)thickening,thickening of left ventricular posterior wall thickness(LVPWs),left ventricular mass(LVM),left ventricular mass and body weight ratio increased at the end of systole,the difference was statistically significant(P<0.05).The left ventricular mass and body weight of the high-salt and low-zinc group were lower than those in the high-salt-high zinc group,and the difference was statistically significant(p<0.05).Considering the difference in body weight between the two groups of rats and the difference in LVM data between the two groups,it is not considered that there is a difference in the degree of ventricular hypertrophy between the two groups.There were no significant differences in the other ultrasound data between the different zinc concentrations.There was no significant difference in ejection fraction(EF)between the groups and left ventricular diameter(LVDs)at the end of systole.The serum BNP was found to be significantly higher in the high salt group than in the normal salt group,and the difference was statistically significant(p<0.05).In the high-salt group comparison,serum BNP levels in the high-zinc group were significantly lower than those in the normal zinc group,and the difference wasstatistically significant(p<0.05).Serum BNP levels in the extremely high zinc and low zinc groups were also lower than those in the normal zinc group,but the difference was not statistically significant.In the determination of myocardial BNP mRNA and protein expression levels,the high salt group was significantly higher than the normal salt group,the difference was statistically significant(p <0.05).The mRNA expression level showed that the high-salt normal zinc group was slightly lower than the other high-salt groups,and the difference was not statistically significant.There was no difference in the expression of high salt histone protein.The results of wet lung/dry lung test in rats were found to be significantly higher in the high-salt diet group than in the control group(p<0.05).The ratio of wet lung/dry lung in high salt normal zinc group and high salt high zinc group was significantly higher than that in high salt high zinc group and high salt low zinc group,and the difference was statistically significant(p<0.05).Combined with the above data,it can be determined that the establishment of HFpEF animal model by DSS rats in this experiment is feasible,but different concentrations of zinc intervention failed to significantly delay or reverse ventricular remodeling.Conclusion1.DSS rats can induce hypertension through high salt feeding to develop HFpEF.2.Changes in dietary zinc concentration alone did not reverse or delay the ventricular remodeling process in HFpEF rats.3.Supplementation of zinc by diet can reduce BNP levels of HFpEF.4.Dietary zinc deficiency may induce obesity in rats,but there is no clear evidence of aggravation of HFpEF. |
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