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去铁酮对酒精性心肌损伤小鼠的保护作用

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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 7 w雄性C57/BL6J小鼠,适应性饲养 1 w,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 10 mL·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 12 w.12 w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(Lactate dehydrogenase,LDH)水平和Fe2+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Fe2+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Fe2+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.
Protective effect of deferiprone on alcoholic-induced myocardial injury in mice
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 Fe2+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 Fe2+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,Fe2+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.

Alcoholic cardiac injuryDeferiproneIron overloadOxidative stress

刘乐、宫利敏、苏娟、徐立、武珺、顾伟

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大理大学医学部基础医学院,云南 大理 671000

大理白族自治州人民医院眼科,云南 大理 671000

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

酒精性心脏损伤 去铁酮 铁过载 氧化应激

2025

四川生理科学杂志
四川省生理科学会

四川生理科学杂志

影响因子:0.575
ISSN:1671-3885
年,卷(期):2025.47(3)