Effect Of Perindopril On FGF-2Expression In Isoproterenol-induced Myocardial Hypertrophy Of Rats

Background and ObjectiveMyocardial hypertrophy is the early pathological changes of various heartdiseases, divided into pathological and physiological, pathological myocardialhypertrophy find expression in myocardial fibers hyperplasia and myocardial cellarranged disorder, continue to develop the cause ventricular remodeling and heartfailure, and could lead to malignant arrhythmia, acute myocardial infarction orsudden cardiac death and so on, it is an independent risk factor for cardiovasculardisease, so the occurrence mechanism of myocardial hypertrophy has always been acardiovascular research hot spot.Fibroblast growth factor is a group of peptide form fiber cell mitogen, canpromote the function of blood vessels, bone formation and damage repair. FGF-1(fibroblast growth factor-1) and FGF-2(fibroblast growth factor-2) was found to bethe earliest, at the same time because of electrophoresis isoelectric point when presentacidic and alkaline is also known as acidic fibroblast growth factor(aFGF/FGF-1) andbasic fibroblast growth factor(bFGF/FGF-2). From overseas research, bFGF andmyocardial cells express functional receptors (FGFR), induced tyrosinephosphorylation cascade, promote the development of myocardial hypertrophy. Fibroblast growth factor2(FGF-2) is a member of the fibroblast growth factorfamily, study abroad show that FGF-2can expressed in chronic renal failure ofmyocardial hypertrophy group increased significantly, prompt FGF-2related to thepathological changes of myocardial hypertrophy.Studies have shown that RAAS system related to the pathological change ofmyocardial hypertrophy. RAAS system that renin-angiotensin-aldosterone system,through the action of renin angiotensinogen converted into angiotensin Ⅰ, Andangiotensin Ⅰformed under the action of angiotensin converting enzyme angiotensinⅡ，then combined with the angiotensin receptor, causing a variety of physiologicaleffects, such as making systemic micro arteries, such as aldosterone secretion,resulting in a number of pathological cardiac remodeling and so on, such as that bodyarteriole contraction, aldosterone secretion to increase, resulting in cardiacremodeling and a series of pathological changes.Angiotensin converting enzymeinhibitors (angiotensin converting enzyme inhibitors, ACEI) drugs can inhibit theangiotensin Ⅰ to angiotensin Ⅱ, reduce angiotensin Ⅱformation, inhibit myocardialremodeling development.This study by subcutaneous injection of isopropyl adrenaline making myocardialhypertrophy rats model, to observe the activities of FGF-2in rat myocardialhypertrophy cell change, explore the FGF-2role in myocardial hypertrophy pathwayand mechanism, and without perindopril split the influence of the expression of FGF-2, provide theoretical basis for future clinical drug treatment.MethodsRandom selection method was applied to30healthy male SD rats were dividedinto control group, model group and drug intervention group,10in each group.Model group and drug intervention group were injected subcutaneously isoproterenol(ISO)3mg/(kg·d) model of myocardial hypertrophy, such as the control group of ratssubcutaneous dose of distilled water. Drug intervention group were perindopril1mg/(kg·d) dissolved in2ml of distilled water orally, control and application of themodel group rats doses of saline, continuous feeding10d.10days to three groups ofrats were used to measure body weight, heart mass and left ventricular mass, and leftventricular mass index calculated heart, the left ventricle were taken three groups HE staining of rat myocardium, left ventricular myocardial morphology and arrangeent ofimmunosuppressive staining observed in myocardial tissue expression of FGF-2,reverse transcriptase polymerase chain reaction (RT-RCR) detection of myocardialcells of FGF-2mRNA levels.Results1Determination of cardiac mass index and left ventricular mass index.①C ardiac mass index(HM/BM):control group<drug intervention group<co-mparison between model group, the group was statistically significant (1.93±0.11mg/g vs2.71±0.34mg/g vs3.79±0.11mg/g, all P<0.05).②Left ventricular massindex(LVM/BM):control group<drug intervention group<model group, the com-parison between groups have statistical significance(1.46±0.11mg/g vs1.96±0.12mg/g vs2.49±0.07mg/g，all P<0.05).2Hematoxylin-eosinstaining stainingControl rule and tidy arrangement of myocardial cell, the structure is clear,no abnormal morphology; Model group myocyte hypertrophy, disordered arran-gement, muscle enlargement of silk texture, interstitial cells showed a large number of myocardial fibers proliferation; The drug intervention group degree ofpathological changes of the myocardial cell is worse than the control group, but better than the model group.3Reverse transcriptase polymerase chain reaction (RT-PCR)Three groups of FGF-2in the left ventricular myocardial tissue of mrnarelative content results: control group<drug intervention group<comparison between model group, the group has statistical significance.(0.39±0.07vs0.63±0.12vs0.73±0.12，all P<0.05)4immunohistochemistryImmunohistochemical staining after FGF-2brown granules in the myocardi-al cells, myocardial cells in normal tissue is a small amount of brown granul-es in the cytoplasm, a weak positive expression; Myocardial cells in model gr-oup of brown can be seen in the cytoplasm, a strong positive expression; Tancan be seen in the intervention group, the positive expression of less than mo-del group.Comparison between groups was statistically significant.Three group s of rats myocardial tissue FGF-2in the positive area average integral opticalde-nsity comparison: control group<drug intervention group<comparison betweenmodel group, the group has statistical significance.(79.41±7.85vs127.11±13.04vs141.07±9.39，all P<0.05).Conclusions1.FGF-2expression in myocardial hypertrophy group increases, prompt FGF-2can promote isopropyl rat myocardial hypertrophy induced by adrenaline.2.FGF-2expression in myocardial tissue of rats which intervention with perindopril was significantly lower than the model group, prompt without perindopril captopril can restrain by lowering the expression of FGF-2ventricular remodeling.