去铁酮对酒精性心肌损伤小鼠的保护作用  

Protective effect of deferiprone on alcoholic-induced myocardial injury in mice

作　　者：刘乐 宫利敏 苏娟 徐立 武珺 顾伟 Liu Le;Gong Li-min;Su Juan;Xu Li;Wu Jun;Gu Wei(School of Basic Medical Sciences,Department of Medicine,Dali University,Dali 671000,Yunnan,China;Department of Ophthalmology,The People's Hospital of Dali Bai Autonomous Prefecture,Dali 671000,Yunnan,China;Yunnan Provincial Clinical Medical Sub-centre for Infectious Diseases,Key Laboratory of Infectious Diseases of Yunnan Provincial Department of Education,Department of Infectious Diseases,The First Affiliated Hospital of Dali University,Dali 671000,Yunnan,China)

机构地区：[1]大理大学医学部基础医学院,云南大理671000 [2]大理白族自治州人民医院眼科,云南大理671000 [3]云南省感染性疾病临床医学分中心,云南省教育厅感染性疾病重点实验室·大理大学第一附属医院感染科,云南大理671000

出　　处：《四川生理科学杂志》2025年第3期473-475,618,共4页

基　　金：2024年度云南省教育厅科学研究基金项目(编号:2024J0857)。

摘　　要：目的:研究去铁酮对酒精诱导的心肌损伤的保护作用及机制。方法:将24只7w雄性C57/BL6J小鼠,适应性饲养1w,按随机数字表法分为对照组、模型组和去铁酮干预组,每组8只。每日以50%酒精10mL·kg^(-1)·d^(-1)灌胃,建立酒精性心肌损伤模型;1 h后,去铁酮干预组给予去铁酮溶液(100 mg·kg^(-1)·d^(-1))灌胃,对照组和模型组给予等剂量生理盐水,整个过程连续12w。12w后经H&E染色观察心脏组织病理变化,采用微量平板法检测小鼠血清、心肌组织乳酸脱氢酶(Lactatedehydrogenase,LDH)水平和Fe^(2+)含量,采用硫代巴比妥酸法检测心肌组织丙二醛(Malondialdehyde,MDA)的含量。结果:与对照组相比,模型组小鼠心肌纤维断裂、溶解,胞外间隙明显增宽,炎细胞浸润;血清、心肌组织LDH水平和Fe^(2+)含量升高;心肌MDA的含量较对照组显著增加(P<0.05)。去铁酮干预后心肌纤维断裂、溶解、胞外间隙等明显改善,少量炎细胞浸润;血清、心肌组织LDH的水平和Fe^(2+)含量及心肌MDA的含量较模型组显著降低(P<0.05)。结论:去铁酮对酒精性心肌损伤小鼠具有保护作用,其机制可能通过抑制心肌细胞铁过载、减轻酒精的氧化应激损伤有关。Objective:To investigate the protective effect and mechanism of deferiprone on alcohol-induced myocardial injury.Methods:Twenty-four male C57/BL6J mice were adaptively fed for 1 week and randomly divided into a control group,a model group,and a deferiprone intervention group using a random number table method,with 8 mice in each group.An alcoholic myocardial injury model was established by orally administering 10 mL•kg^(-1)•d^(-1) of 50%alcohol daily.After 1 hour,the intervention group was given deferiprone solution(100 mg•kg^(-1)•d^(-1))by gavage,while the control group and model group were given equal doses of physiological saline.After 12 weeks,the pathological changes in heart tissue were observed by H&E staining.The levels of lactate dehydrogenase(LDH)and Fe^(2+)in mouse serum and myocardial tissue were detected by microplate assay,and the content of malondialdehyde(MDA)in myocardial tissue was detected by thiobarbituric acid assay.Results:Compared with the control group,the model group mice showed myocardial fiber rupture and dissolution,significant widening of extracellular spaces,infiltration of inflammatory cells,and elevated levels of LDH and Fe^(2+)in serum and myocardial tissue.The content of myocardial MDA significantly increased compared to the control group(P<0.05).After intervention with deferiprone,myofibril fiber rupture,dissolution,extracellular space,and a small amount of inflammatory cell infiltration were significantly improved.The levels of serum and myocardial tissue LDH,Fe^(2+)content,and myocardial MDA content were significantly reduced compared to the model group(P<0.05).Conclusion:Deferiprone has a protective effect on alcoholic myocardial injury in mice,and its mechanism may be related to inhibiting myocardial cell iron overload and reducing alcohol induced oxidative stress damage.

关 键 词：酒精性心脏损伤 去铁酮 铁过载 氧化应激 

分 类 号：R28[医药卫生—中药学]