蛋白质羰基化与大鼠心衰恶病质发生的相关性

目的 探讨蛋白质羰基化是否参与了大鼠心衰恶病质的发生、发展。方法 90只12个月龄的清洁级雄性 SD大鼠，随机分为异丙肾上腺素（ISO）组、肼苯哒嗪（HYD）+ISO组和对照组，每组各30只。分别给予ISO组和HYD+ ISO组大鼠注射异丙肾上腺素，同时HYD+ISO组大鼠用肼苯哒嗪灌胃，对照组注射生理盐水。6周后，根据大鼠的超 声心动图和体质量的变化评估大鼠造模成功率。采用全自动生化分析仪检测大鼠血清中总白蛋白、三酰甘油、胆固 醇、血糖水平；酶联免疫吸附测定试剂盒测定大鼠血清中的脑钠肽（BNP）的水平；紫外分光光度计检测心肌及骨骼肌 中蛋白质羰基水平；免疫组化染色检测心肌及骨骼肌中蛋白质羰基表达情况。结果 对照组、HYD+ISO组及ISO组 血清总白蛋白及血糖依次降低，血清三酰甘油、胆固醇、BNP、心肌和骨骼肌中蛋白质羰基浓度依次升高（P＜0.05）， 大鼠心肌和骨骼肌中蛋白质羰基化阳性细胞百分率依次增高（P＜0.05）。结论 ISO所致的心衰恶病质大鼠模型蛋 白质羰基化水平升高；HYD会抑制心衰恶病质大鼠体内蛋白质羰基化的形成，可阻止心衰恶病质的发生、发展。

Correlation between protein carbonylation and the heart failure cachexia in rats

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.