Ghrelin 肽对盐酸多柔比星诱导的大鼠心力衰竭的保护作用。
The protective effect of Ghrelin peptide on doxorubicin hydrochloride induced heart failure in rats.
机构信息
Department of Cardiology, Jiangxi Provincial People's Hospital, the First Affiliated Hospital of Nanchang Medical College, Nanchang, 330006, Jiangxi Province, China.
Department of Neurology, Jiangxi Provincial People's Hospital, the First Affiliated Hospital of Nanchang Medical College, Nanchang, 330006, Jiangxi Province, China.
出版信息
J Cardiothorac Surg. 2024 Sep 2;19(1):508. doi: 10.1186/s13019-024-02994-3.
BACKGROUND
To investigate the protective effect and mechanism of Ghrelin on Doxorubicin (Dox) hydrochloride induced heart failure (HF) and myocardial injury in rats.
METHODS
45 rats were randomly divided into control group, HF group and Ghrelin group. Dox hydrochloride was injected intraperitoneally to establish the model of HF in rats of HF group and Ghrelin group. Rats in the Ghrelin group were given intraperitoneal injection of Ghrelin twice a day, and rats in the HF group and control group were given equal volume of normal saline for a total of 6 weeks. The changes of echocardiography, cardiac hemodynamics, myocardial histology and plasma inflammatory factors were observed.
RESULTS
After the Ghrelin intervention, compared with the HF group, the left ventricular end-diastolic diameter (LVDD) and left ventricular end-systolic diameter (LVSD) in the Ghrelin group was markedly reduced (P < 0.05), and left ventricular ejection fraction (LVEF) was significantly increased (P < 0.05). Compared with HF group, the left ventricular systolic pressure (LVSP), maximum rate of increase in left ventricular pressure (+ dP/dtmax) and maximum rate of decrease in left ventricular pressure (- dP/dtmax) of Ghrelin group was remarkedly increased (P < 0.05), left ventricular diastolic pressure (LVDP) decreased (P < 0.05). In the Ghrelin group, the degree and extent of cardiomyocyte degeneration and necrosis were remarkedly reduced compared with the HF group. The levels of TNF-α and iNOS in Ghrelin group were notably lower than those in HF group (P < 0.05), the IL-10 level increased markedly (P < 0.05).
CONCLUSION
Ghrelin may reduce Dox-induced myocardial injury and improve cardiac function in rats by regulating inflammation and oxidative stress.
背景
研究 Ghrelin 对盐酸多柔比星（Dox）诱导的大鼠心力衰竭（HF）和心肌损伤的保护作用及机制。
方法
将 45 只大鼠随机分为对照组、HF 组和 Ghrelin 组。HF 组和 Ghrelin 组大鼠腹腔注射盐酸多柔比星建立 HF 模型，Ghrelin 组大鼠每天腹腔注射 Ghrelin 2 次，HF 组和对照组大鼠给予等体积生理盐水，共 6 周。观察各组大鼠超声心动图、心脏血流动力学、心肌组织学及血浆炎症因子的变化。
结果
Ghrelin 干预后，与 HF 组比较，Ghrelin 组大鼠左心室舒张末期直径（LVDD）和左心室收缩末期直径（LVSD）明显减小（P<0.05），左心室射血分数（LVEF）明显升高（P<0.05）。与 HF 组比较，Ghrelin 组大鼠左心室收缩压（LVSP）、左心室压力最大上升速率（+ dP/dtmax）和左心室压力最大下降速率（- dP/dtmax）明显升高（P<0.05），左心室舒张压（LVDP）降低（P<0.05）。Ghrelin 组大鼠心肌细胞变性、坏死程度及范围较 HF 组明显减轻。Ghrelin 组大鼠肿瘤坏死因子-α（TNF-α）和诱导型一氧化氮合酶（iNOS）水平明显低于 HF 组（P<0.05），白细胞介素-10（IL-10）水平明显升高（P<0.05）。
结论
Ghrelin 可能通过调节炎症和氧化应激，减轻 Dox 诱导的大鼠心肌损伤，改善心功能。
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