Effect Of NLRP3 Inflammatory Bodies On Cardiac Hypertrophy Induced By Angiotensin Ⅱ

Objective The aim of this study was to investigate the effect of nucleotide binding oligomeric domain-like receptor protein 3(NLRP3)on cardiac hypertrophy induced by angiotensin Ⅱ(AngⅡ)in mice.Methods Twenty-four 8-week-old male C57BL/6 mice weighing 24-26g were randomly divided into three groups:nonnal control group(control group),angiotensinⅡ+ saline group(AngⅡ group)and angiotensin Ⅱ+ NLRP3 inhibitor group(NLRP3 inhibitor group)with 8 mice in each group.The mini osmotic release pump was implanted subcutaneously in all groups of mice.Both the Ang Ⅱ group and the NLRP3 inhibitor group were subcutaneously injected with Ang Ⅱ solution of 5mg/ml at the rate of 0.26ml/kg/days,while the mice in the control group were continuously pumped with normal saline for 0.26ml/kg/days.During this period,the mice in the NLRP3 inhibitor group were injected intraperitoneally with NLRP3 inhibitor MCC950 solution of 0.35mg/ml at the concentration of 10 ml/g every other day,and the mice in the control group and Ang Ⅱ group were intraperitoneally injected with 10ul/g saline every other day.After 4 weeks of observation,the mice were weighed,the mice were killed and the heart was removed by rapid thoracotomy,and the whole heart weight was weighed,and the heart mass index[heart mass(mg)/body weight(g),HMI]was calculated.The ventricle is divided into three equal segments-the upper segment,the middle segment and the inferior segment.The BNP、β-MHC mRNA expression of cardiomyocytes in the upper segment of the ventricle was detected by Quantitative Real-time polymerase chain reaction(RT-qPCR)method,and the myocardial collagen fiber content and cross-sectional area of cardiomyocytes were detected by Masson(Masson)staining and hematoxylin-eosin(HE)staining respectively.Results1 Changes of cardial hypertrophy and collagen fiber content in mice1.1 Changes in heart mass index(HMI)of mice in each group The HMI of AngⅡgroup was higher than that in the control group[(5.20±0.18)ratio(4.14±0.21)mg/g,P<0.05];there was no significant difference in HMI between NLRP3 inhibitor group and AngⅡ group.[(5.19±0.47)ratio(5.20±0.18)mg/g,P>0.05]1.2 Changes in cross-sectional area of cardiomyocytes of mice in each group The cross-sectional area of myocardial cells in AngⅡ group was larger than that in control group[(384.57±91.53)ratio(285.38±59.60)um2,P<0.05];there was no significant difference in the cross-sectional area of cardiomyocytes between the NLRP3 inhibitor group and the AngⅡ group[(373.66±94.16)ratio(384.57±91.53)um2,P>0.05].1.3 Changes in myocardial collagen fiber volume fraction of mice in each group The volume fraction of myocardial collagen fibers in AngⅡ group was higher than that in control group[(15.64±1.53)ratio(5.44±1.27)%,P<0.05];there was no significant difference in the volume fraction of myocardial collagen fibers between the NLRP3 inhibitor group and the AngⅡ group[(15.85±2.53)ratio(15.64±1.53)%,P>0.05].2 Changes of BNP mRNA expression level in myocardial cells of mice The expression level of BNP mRNA in AngⅡ group was higher than that in control group[(1.64±0.21)to 1,P<0.05];there was no significant difference in the expression level of BNP mRNA between the NLRP3inhibitor group and the AngⅡ group[(1.46±0.15)ratio(1.64±0.21),P>0.05].3 Changes of β-MHC mRNA expression level in myocardial cells of mice The expression level of β-MHC mRNA in AngⅡ group was higher than that in control group[(1.48±0.22)to 1,P<0.05];there was no significant difference in the expression level of β-MHC mRNA between the NLRP3inhibitor group and the AngⅡ group[(1.48±0.22)ratio(1.61 ±0.25),P>0.05].3 Conclusions1.AngⅡ can induce cardiac hypertrophy in mice,and collagen fibers in cardiac hypertrophy increase.2.NLRP3 was not associated with AngⅡ-induced cardiac hypertrophy.