This study was designed to investigate the effects and mechanism of the GCIP-27 polypeptide drug on heart function in rats challenged with Dox that induces CHF. Several studies have demonstrated a beneficial effect of the GCIP-27 polypeptide on cardiac hypertrophy induced by a variety of factors in vivo and in vitro. Cardiac hypertrophy is an important factor in the development of CHF. Cardiac hypertrophy is typically believed to be a compensatory mechanism of the heart in response to increased systemic demand for cardiac output. Given this premise, preventing or reversing ventricular remodeling might impair heart function during the compensatory stage and the heart GDC-0941 failure stage. As GCIP-27 may reduce cardiac hypertrophy, it becomes important to determine whether GCIP-27 is beneficial to heart functioning during CHF. In this study, GCIP-27 treatment was shown to markedly increase body weight, improve survival, and halt the process of hypertrophy and heart failure in doxorubicin-induced CHF rats, preventing adverse ventricular remodeling imposed by Dox. Due to the cardiac toxicity and other adverse effects of doxorubicin, rats receiving Dox may eat less and gain less body weight. Along with the decrease of the heart function, concentration of plasmic catecholamine, such as norepinephrine increase significantly, which can reduce appetite and food intake through ��1-adrenoceptor. GCIP-27 is a synthetic peptide, which imitate the structure of carboxyl terminus of Gq protein �� subunit and can inhibit the signal transduction of the Gq-coupled receptors including ��1-adrenoceptor. Therefore, GCIP-27 not only ameliorated heart function but also increased food intake and body weight. Similarly, losartan can reduce afterload of the heart and improve heart function through blocking angiotensin II type 1 receptor, and subsequently decrease catecholamine and reduce body weight loss. Additionally, it has been shown that GCIP-27 was superior at inhibiting ventricular remodeling compared with losartan. In the Epoxomicin present study, B-mode and M-mode echocardiography revealed that GCIP-27 was able to improve heart function. These results indicated that this polypeptide drug produced favorable effects on doxorubicin-induced CHF in rats. Although GCIP-27could lower blood pressure in spontaneously hypertensive rats, the hypotensive effect of GCIP-27 is significant weaker than that of losartan. And due to compensation, the normotensive animals, such as rats, dogs and patients, are less sensitive to hypotensive agents, such as losartan and nitroprusside, etc., than hypertensive subjects. We have also ever observed that GCIP-27 had no influence on the blood pressure in normotensive rats. In doxorubicin- induced heart failure rats, blood pressure and hemodynamic parameters showed a slight decrease or no change. Therefore, the hemodynamics factors contributed not as much as remodeling to the mechanism for GCIP-27-induced improvement of heart function. In the current study, chloral hydrate was used to anesthetize the rats before measuring cardiac function and tissue collection. Although chloral hydrate has various adverse effects, such as not providing analgesia, prolonging recovery time after surgery, inducing mutagenesis and carcinogenesis, it is considered by some a good sedative-hypnotics for animals. Experimental anesthesia based on an intraperitoneal injection of chloral hydrate is believed to have minimal effects on cardiovascular function or reflexes, while ketamine and pentobarbital sodium can lead to a significant decrease in heart function indexes and survival rate. Therefore, chloral hydrate is occasionally still used as an anesthetic agent in the laboratory.