The Research Of Relationship Between TLR4/MyD88 Protein Expression With AngⅡ Induced Myocardi L Hypertrophy

Objective to study the protein expression level of TLR4 / MyD88 relations with AngⅡ induced myocardial hypertrophyMethods select 21 only 8-10 weeks of C57 BL / 6 male mice,were randomly divided into three groups: normal control group(control group),myocardial hypertrophy group(hereinafter referred to as hypertrophy group),myocardial hypertrophy,drug intervention group(hereinafter referred to as intervention group),each group of seven.Three groups all subcutaneous preparetions osmotic pump,the control group at a speed of 1.3 mg/Kg/day continuous pumping physiological saline,hypertrophy and hypertrophy intervention group at a speed of 1.3 mg/Kg/day continuous pumping AngⅡ;Control group with hypertrophy group 2 times per week during intraperitoneal injection of saline,hypertrophy TAK242 produced by intraperitoneal injection of intervention group 2 times a week.Observation to be put to death in mice after 4 weeks,low temperature fast heart,put in precooling ahead of physiological saline,gently squeeze out the heart cavity blood,after repeated 2-3times sterile gauze blot moisture heart,heart at its widest point and apex as the point of tangency,the heart is divided into three parts,including ventricular upper segment by real-time fluorescent Quantitative PCR(policy Real-time PCR,RT-qPCR)by RNA extraction,reverse transcription,cDNA amplification process detection beta myosin heavy chain(beta-myosin heavy chain,beta MHC)m RNAexpression;Ventricular midway in the fore Ma Linzhong fixed by routine paraffin section after dehydration,transparent,embedding with hematoxylin-eosin staining method(hematoxylin-eosin staining,HE)to observe the myocardial cell morphology;Apex of protein immunoblot(Western Blot,WB)extracted by protein,electrophoresis,transfer film,closed,a fight incubation,two fight incubation,chemiluminescence detection of TLR4,developing and fixing process and MyD88 protein expression level.Statistical software SPSS20.0 was used for data analysis,and p<0.05 was considered as a statistically significant difference.Results1 the myocardial cell morphological changes of miceMyocardial hypertrophy group cross cut area significantly greater than the control group(3710.21 + /-378.45 vs1804.35 plus or minus 310.18,P < 0.01),cross-sectional area of myocardial cells in mice hypertrophy intervention group was obviously less than hypertrophy group(3125.14 + /-734.46 vs.3710.21 + /-378.45,P < 0.01).2 the expression of Beta MHC mRNAMyocardial hypertrophy group beta cells MHC m RNA expression level was higher than control group(P < 0.05),after intervention to TAK242 hypertrophy rat cardiomyocytes beta MHC mRNA expression were inhibited(P < 0.05).3 the expression of TLR4 and MyD88 levelin Each groupmyocardial cells Hypertrophy of cardiac muscle cells the expression of TLR4 and MyD88 levels higher than the control group(TLR4: P < 2.76 0.05),after intervention to TAK242 hypertrophy rat cardiomyocytes TLR4,MyD88 protein expression levels(P < 0.05).Conclusion1.In the myocardial hypertrophy induced by AngⅡ,TLR4 and MyD88 protein expression level increased.2.TAK242 intervention inhibiting TLR4 and MyD88 protein expression level,improved the degree of myocardial hypertrophy,TLR4,MyD88 participate in thedevelopment process of myocardial hypertrophy.