1.武汉大学人民医院心血管内科/代谢与相关慢病湖北省重点实验室 湖北 武汉 430060
2.中国中医科学院西苑医院 北京 100091
张欣茹,女,2001—,医学硕士生,主要从事心血管疾病的研究,E⁃mail:zhangxinru@whu.edu.cn。
高铸烨,E⁃mail:zhuyegao@126.com
唐其柱,E⁃mail:qztang@whu.edu.cn。
收稿:2025-11-28,
纸质出版:2026-10-25
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张欣茹,姜众会,高铸烨等.苦参酮对心脏缺血再灌注诱导心肌重构的影响和机制[J].武汉大学学报(医学版),2026,47(10):1295-1301.
ZHANG Xinru,JIANG Zhonghui,GAO Zhuye,et al.Effects and mechanisms of kurarinone on myocardial remodeling induced by cardiac ischemia⁃reperfusion[J].Medical Journal of Wuhan University,2026,47(10):1295-1301.
张欣茹,姜众会,高铸烨等.苦参酮对心脏缺血再灌注诱导心肌重构的影响和机制[J].武汉大学学报(医学版),2026,47(10):1295-1301. DOI: 10.14188/j.1671-8852.2025.1458.
ZHANG Xinru,JIANG Zhonghui,GAO Zhuye,et al.Effects and mechanisms of kurarinone on myocardial remodeling induced by cardiac ischemia⁃reperfusion[J].Medical Journal of Wuhan University,2026,47(10):1295-1301. DOI: 10.14188/j.1671-8852.2025.1458.
目的
2
探讨苦参酮(KAR)对心脏缺血再灌注损伤(MIRI)诱导心肌重构的作用及分子机制。
方法
2
构建小鼠心脏缺血再灌注模型,将小鼠随机分为4组,即假手术+工作液给药组(Sham+Veh)、Sham+苦参酮给药组(Sham+KAR)、缺血再灌注+工作液给药组(I/R+Veh)、I/R+苦参酮给药组(I/R+KAR)。假手术或I/R手术后7 d为造模终点,取小鼠心脏和血清进行病理和生化分析。测量心脏大体和心功能指标;试剂盒检测心肌损伤标志物水平;HE染色、WGA染色观察心肌细胞形态学变化;PSR染色检测心肌纤维化水平;TUNEL染色评估心肌细胞凋亡;Western Blot检测心肌氧化应激相关蛋白的表达水平。
结果
2
KAR显著改善小鼠MIRI后的心功能和梗死范围(
P
<
0.05);缓解MIRI小鼠心脏结构紊乱,减轻心脏重构(
P
<
0.05);降低MIRI小鼠的心脏氧化应激水平和凋亡(
P
<
0.05)。机制上,KAR通过上调Nrf2蛋白水平,促进下游抗氧化基因SOD2、HO⁃1的表达。
结论
2
苦参酮通过调控Nrf2/HO⁃1通路,改善心肌缺血再灌注后的心肌重构和氧化应激损伤。
Objective
2
To explore the effect and molecular mechanism of kurarinone (KAR) on myocardial remodeling induced by myocardial ischemia‑reperfusion injury (MIRI).
Methods
2
Mouse models of myocardial ischemia‑reperfusion (I/R) were constructed
and the mice were randomly divided into four groups: sham operation + vehicle group (Sham+Veh)
sham operation + KAR group (Sham+KAR)
I/R + vehicle group (I/R+Veh)
and I/R + KAR group (I/R+KAR). The endpoint was set at 7 days after sham or I/R operation
and mouse hearts and serum were collected for pathological and biochemical analysis. Gross cardiac morphology and cardiac function were assessed. Commercial assay kits were used to detect serum levels of myocardial injury markers. HE staining and wheat germ agglutinin (WGA) staining were used to observe cardiomyocyte morphological changes. Picro sirius red (PSR) staining was used to evaluate the degree of myocardial fibrosis. TUNEL staining was used to assess cardiomyocyte apoptosis. Western blot was used to detect the expression of myocardial oxidative stress‑related proteins.
Results
2
KAR significantly improved cardiac function and reduced infarct size in mice after MIRI (
P
<
0.05)
alleviated myocardial structural damage and attenuated cardiac remodeling (
P
<
0.05)
and decreased oxidative stress and cardiomyocyte apoptosis (
P
<
0.05). Mechanistically
KAR promoted the expression of downstream antioxidant genes SOD2 and HO‑1 by upregulating Nrf2 protein expression.
Conclusion
2
Kurarinone ameliorates myocardial remodeling and oxidative stress injury after myocardial ischemia‑reperfusion by regulating the Nrf2/HO‑1 pathway.
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