[1]卢素贤 郭慈航 王顺 鲁志兵.限时进食通过抑制细胞铁死亡减轻脓毒性心肌损伤[J].心血管病学进展,2025,(12):1131.[doi:10.16806/j.cnki.issn.1004-3934.2025.12.015]
　LU Suxian,GUO Cihang,WANG Shun,et al.Time-Restricted Feeding Alleviates Sepsis-Induced Myocardial Injury via Inhibition of Cellular Ferroptosis[J].Advances in Cardiovascular Diseases,2025,(12):1131.[doi:10.16806/j.cnki.issn.1004-3934.2025.12.015]
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限时进食通过抑制细胞铁死亡减轻脓毒性心肌损伤()

《心血管病学进展》[ISSN:51-1187/R/CN:1004-3934]

卷:
期数:
2025年12期
页码:
1131
栏目:
论著
出版日期:
2025-12-25

文章信息/Info

Title:
Time-Restricted Feeding Alleviates Sepsis-Induced Myocardial Injury via Inhibition of Cellular Ferroptosis
作者:
卢素贤 郭慈航 王顺 鲁志兵
(武汉大学中南医院心血管内科/武汉大学心肌损伤与修复研究所 湖北省心血管病介入诊疗临床医学研究中心, 湖北 武汉 430071)
Author(s):
LU Suxian; GUO Cihang; WANG Shun; LU Zhibing
(Department of Cardiology,Zhongnan Hospital,Wuhan University,Institute of Myocardial Injury and Repair,Wuhan University,Hubei Provincial Clinical Research Center for Cardiovascular Intervention,Wuhan 430071,Hubei,China)
关键词:
限时进食; 炎症; 脓毒性心肌病; 细胞铁死亡; 热量限制
Keywords:
Time-restricted feeding; Inflammation; Sepsis-induced cardiomyopathy; Ferroptosis; Calorie restriction
DOI:
10.16806/j.cnki.issn.1004-3934.2025.12.015
摘要:
目的 探讨限时进食（TRF）对脂多糖（LPS）诱导的小鼠心肌损伤的影响。方法 小鼠6周龄开始随机分为正常喂养组（NF组）和TRF组，喂养4周后，于建模前将小鼠随机分为4组，NF+磷酸盐缓冲液（PBS）组（n＝6）、TRF+PBS组（n＝6）、NF+LPS组（n＝10）、TRF+LPS组（n＝10），前两组小鼠给予腹腔注射PBS，后两组给予腹腔注射LPS（50 mg/kg）来构建脓毒性心肌损伤模型。为评估心肌损伤程度，给药6 h 后，使用小动物超声评估各组小鼠心脏功能，12 h 后采集小鼠血清检测心肌损伤标志物及炎症因子，心脏组织进行HE染色评估心肌组织形态。通过蛋白质印迹法检测细胞铁死亡相关指标。为进一步验证TRF通过影响细胞铁死亡减轻LPS诱导的心肌损伤，再次重复上述喂养方法，于建模前，将小鼠随机分为NF+PBS组（n＝6）、NF+LPS组（n＝6）、TRF+LPS组（n＝10）及TRF+LPS+细胞铁死亡诱导剂（erastin）组（n＝10），除NF+PBS外，其余三组建模方法同上。采用上述方法再次评估心肌损伤程度及检测细胞铁死亡诱导情况。结果 （1）与NF+PBS组相比，NF+LPS组表现为小鼠心脏功能下降，小鼠的左室射血分数和左室短轴缩短率均下降，心肌损伤标志物、心肌炎症因子水平及细胞铁死亡均增加；（2）与NF+LPS组相比，TRF+LPS组可以通过降低细胞铁死亡水平来减轻心肌炎症，从而改善小鼠心脏功能；（3）与TRF+LPS组相比，TRF+LPS+erastin组显著抑制了TRF对脓毒性心肌病心肌损伤的保护作用。结论 TRF可以通过抑制细胞铁死亡来减轻脓毒性心肌损伤。
Abstract:
Objective To investigate the effects of time-restricted feeding (TRF) and ferroptosis on lipopolysaccharide (LPS)-induced myocardial injury in a murine model of sepsis-induced cardiomyopathy. Methods Six-week-old mice were randomized into normal feeding (NF) or TRF groups for 4 weeks. Prior to modeling,mice were further subdivided into four groups:NF+PBS (n＝6),TRF+PBS (n＝6),NF+LPS (n＝10),and TRF+LPS (n＝10). Sepsis-induced cardiomyopathy was induced by intraperitoneal injection of LPS (50 mg/kg) or PBS. Cardiac function was assessed by echocardiography 6 hours post-injection. At 12 hours,serum samples were collected to measure myocardial injury biomarkers and inflammatory cytokines,while myocardial damage was histologically evaluated using hematoxylin-eosin (HE) staining. Ferroptosis-related proteins were analyzed by Western blotting.To further verify the role of TRF in ferroptosis regulation,a secondary experiment was performed with the following groups:NF+PBS (n＝6),NF+LPS (n＝6),TRF+LPS (n＝10),and TRF+LPS+erastin (a ferroptosis inducer,n＝10). Cardiac function and ferroptosis markers were re-evaluated using the same protocols. Results (1)Compared with the NF+PBS group,the NF+LPS group showed impaired cardiac function,characterized by decreased ejection fraction (EF) and fractional shortening (FS),along with increased levels of myocardial injury biomarkers,pro-inflammatory cytokines,and ferroptosis.(2)Compared with the NF+LPS group,the TRF+LPS group exhibited reduced myocardial inflammation and ferroptosis,thereby improving cardiac function.(3)Compared with the TRF+LPS group,the TRF+LPS+erastin group markedly abrogated the cardioprotective effects of TRF against sepsis-induced cardiomyopathy (SCM).Conclusion T RF attenuates LPS-induced septic cardiomyopathy by inhibiting ferroptosis,suggesting a potential dietary intervention strategy for sepsis-associated myocardial injury

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更新日期/Last Update: 2026-04-14