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Chronic heart failure (chronic heart failure, CHF) is a variety of causes myocardial structural and functional changes caused by a complex clinical syndrome characterized by ventricular pump dysfunction, is the end stage of a variety of cardiovascular diseases. Prevent the development of heart failure, and reduce the mortality rate has become a major key issues of prevention and treatment of cardiovascular disease. In recent years, the gradual deepening of the the pathophysiological process research of chronic heart failure, the understanding of its pathogenesis from the liquid retention, pump dysfunction, neuroendocrine excessive activation of the cytokine system, the gradual development of myocardial remodeling. Myocardial remodeling in heart failure, the development of important molecular cytological basis, and thus for the treatment of heart failure has been the traditional \Compensatory myocardial hypertrophy in chronic heart failure process helps increase myocardial contractility and increase cardiac output and loss of compensatory hypertrophy is caused by the increase in myocardial oxygen consumption and worsening heart failure. Anti-myocardial remodeling treatment is bound to affect cardiac function. Advantage Xin Kang (huilixinkang, HLXK) the my room for a G protein Gq protein α subunit clones prepared inhibitory peptide drug, previous studies have confirmed, HLXK effective inhibition of angiotensin (angiotensin, Ang) II, to vitro myocardial cell hypertrophy induced by noradrenaline (norepinephrine, NE) reaction, prevention and treatment of a variety of different animal models of left ventricular remodeling, inhibit monocrotaline-induced right ventricular remodeling. Given the myocardial remodeling in the pathogenesis of chronic heart failure, as well as an important role in the prognosis Influence of research HLXK with CHF is necessary. Methods: Animal grouping and model to establish: healthy and clean 48 SD male rats weighing 200 to 220g, were randomly divided into control group, model group, losartan group of (6mg/kg, ig, qd) HLXK ( 10,30,90 μg / kg, ip, bid) group (n = 8). Increments of 15 days of the doxorubicin dose intraperitoneal injection prepared rats with chronic heart failure model, administered separately by subgroups, continuous 10w; experiment, close observation of the general condition of the rats and death. All animals were weighed every four days time, and as a basis for adjusting the dose; 3 after the last administration, the application of high-frequency color ultrasound diagnostic apparatus, measurement of left ventricular diastolic diameter (LVDD), contraction end systolic diameter (LVSD), left ventricular end-diastolic wall thickness (LVPWD) systolic wall thickness (LVPWS), left atrial (LA); calculated left ventricular end-diastolic volume (LVEDV), end-systolic volume (LVESV) , stroke volume (SV), ejection fraction (EF) and fractional shortening rate (FS); 4 weighing Determination HW, LVW; HE staining, light microscopy pathomorphology; Real-time PCR detection alpha-MHC mRNA in myocardial tissue, β-MHC mRNA and Brg1 mRNA expression levels; immunohistochemical method of detection of left ventricular α-MHC, β-MHC, Bcl-2 and Bax protein to detect Brg1, p-; Western blot ERK1 / 2, PKCε and PKCβ Ⅱ protein expression; 5. using fixed-P method and chemiluminescence determination of the SERCA2a activity of cardiac sarcoplasmic reticulum, plasma troponin I levels. Results: 1 control group rat fur smooth and shiny, the spirit of good eating movable; heart failure model rats gradually listlessness, hair removal, less active, slow weight gain; while the administration treated rats 'Basic, the spirit, the weight growth close to the control group; and doxorubicin significantly induced rats with chronic heart failure. HLXK (30,90 μg / kg) can significantly improve the myocardial tissue injury of rats with heart failure and reduced cardiac index and left ventricular index, to improve cardiac ejection fraction and fractional shortening; 3.HLXK (30, 90, μg / kg) significantly increased α-MHC expression in rats with chronic heart failure, and reduce the expression of β-MHC and Brg1; 4.HLXK (30,90 μg / kg) treatment significantly enhanced the activity of chronic heart failure rat cardiac sarcoplasmic reticulum SERCA2a reduce plasma troponin I levels; 5.HLXK (30,90 μg / kg) can significantly improve the chronic heart failure rat PKCε p-ERK1 / 2 and the expression of Bcl-2 protein, reduce PKCβ II, Bax expression. Conclusion: 1.Gq protein α subunit carboxy-terminal mimetic peptide willy heart health can effectively improve the heart function of rats with chronic heart failure, reduce the myocardial tissue injury, inhibit left ventricular remodeling; 2. Willy heart health by myocardial cells raised Bc1-2, downregulation of Bax expression, mitochondrial protect myocardial cells inhibit left ventricular myocardial apoptosis; willy Xinkang anti-heart failure and cut Brg1 expression correct α-MHC and β-MHC, and PKCβ Ⅱ the PKCε imbalance raised the ERK1 / 2 activity, enhanced SERCA2a activity of the cardiac sarcoplasmic reticulum, inhibition of cardiomyocyte apoptosis.
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