Abstract: Objective To investigate whether protein carbonylation was involved in the development of heart failure cachexia in rats. Methods Ninety 12-month-old clean male Sprague-Dawley rats were randomly divided into three groups: isoproterenol (ISO) group, hydralazine (HYD) + ISO group and control group, 30 in each group. Rats in the ISO group and the HYD+ISO group were injected with isoproterenol, the rats in the HYD+ISO group were orally administered with hydralazine, and the rats of control group were injected with normal saline. After 6 weeks, the rat modelling success rate was evaluated based on the echocardiogram and body weight changes. The serum levels of total albumin, triglyceride, cholesterol and blood glucose concentrations in rats were detected by automatic biochemical analyzer. The serum concentration of brain natriuretic peptide (BNP) was detected by ELISA kit. UV spectrophotometer was used to detect protein carbonyl concentration. The immunohistochemistry was used to detect the expression of protein carbonyl. Results In the control group, HYD+ISO group and ISO group, the serum levels of total albumin and blood glucose decreased in turn, and the serum levels of triglyceride, cholesterol, BNP, protein carbonyl in myocardium and skeletal muscle increased in turn (P＜0.05). Conclusion In the rat model of heart failure cachexia caused by ISO, protein carbonylation is elevated. HYD can inhibit the formation of protein carbonylation in rats with heart failure cachexia, which may prevent the occurrence and development of heart failure cachexia.

Key words: heart failure cachexia, protein carbonylation, oxidative stress, brain natriuretic peptide