鸢尾苷通过抗炎及抗氧化应激改善急性心肌梗死后的心肌损伤

范浩淼; 李养; 王晨阳; 赵宇航; 周建良

doi:10.14188/j.1671-8852.2026.0011

您当前的位置：

首页 >

文章列表页 >

鸢尾苷通过抗炎及抗氧化应激改善急性心肌梗死后的心肌损伤

中药活性成分在心血管疾病中的作用机制研究 | 更新时间：2026-11-05

- 鸢尾苷通过抗炎及抗氧化应激改善急性心肌梗死后的心肌损伤
- Tectoridin ameliorates myocardial injury after acute myocardial infarction through anti‐inflammatory and antioxidant stress mechanisms
- 武汉大学学报（医学版） 2026年47卷第10期页码：1318-1324
- 作者机构：
  
  武汉大学中南医院心血管外科湖北武汉 430071
- 作者简介：
  
  范浩淼，男，2001—，医学硕士，从事心血管基础研究，E‐mail：18303763546@163.com。
  周建良，E‐mail：zjl20210802@whu.edu.cn。
- 基金信息：
  
  国家自然科学基金面上项目(82270382);湖北省自然科学基金项目(2023AFC040)
- DOI：10.14188/j.1671-8852.2026.0011
  中图分类号： R54
- 收稿：2026-01-05，
  
  纸质出版：2026-10-25
- 稿件说明：
移动端阅览
范浩淼,李养,王晨阳等.鸢尾苷通过抗炎及抗氧化应激改善急性心肌梗死后的心肌损伤[J].武汉大学学报（医学版）,2026,47(10):1318-1324.

FAN Haomiao,LI Yang,WANG Chenyang,et al.Tectoridin ameliorates myocardial injury after acute myocardial infarction through anti‐inflammatory and antioxidant stress mechanisms[J].Medical Journal of Wuhan University,2026,47(10):1318-1324.
范浩淼,李养,王晨阳等.鸢尾苷通过抗炎及抗氧化应激改善急性心肌梗死后的心肌损伤[J].武汉大学学报（医学版）,2026,47(10):1318-1324. DOI： 10.14188/j.1671-8852.2026.0011.

FAN Haomiao,LI Yang,WANG Chenyang,et al.Tectoridin ameliorates myocardial injury after acute myocardial infarction through anti‐inflammatory and antioxidant stress mechanisms[J].Medical Journal of Wuhan University,2026,47(10):1318-1324. DOI： 10.14188/j.1671-8852.2026.0011.

摘要

目的

探究鸢尾苷(Tectoridin)对心肌梗死后心肌损伤的影响及其作用机制。

方法

通过结扎小鼠冠状动脉左前降支构建心肌梗死模型，采用小动物超声心动图评估心功能[左心室射血分数（EF）、短轴缩短率（FS）]，TTC染色量化梗死面积，免疫荧光检测GR1细胞浸润，实时荧光定量PCR分析炎症因子(IL‐6、TNF‐α、IL‐1β)的mRNA表达，蛋白印迹检测凋亡蛋白(Bax、Bcl2)及抗氧化蛋白(Sod2、Nrf2、Ho‐1)水平。通过Nrf2敲除小鼠模型验证靶点特异性。

结果

鸢尾苷显著改善心肌梗死后EF值，从MI组的28.4%提升至鸢尾苷组的38.5%（

0.01)，梗死面积减少约21%，抑制GR1细胞浸润及炎症因子表达，并上调抗氧化蛋白(Sod2、Nrf2、Ho‐1)。机制上，鸢尾苷通过促进Nrf2核转位激活抗氧化通路，减少活性氧积累和细胞凋亡(Bax/Bcl2比值下降)。Nrf2敲除后，鸢尾苷的心肌保护作用被消除，证实Nrf2是其关键分子靶点。

结论

鸢尾苷通过激活Nrf2/Ho‐1通路，减轻氧化应激、抑制炎症与凋亡，从而改善心肌梗死后的心脏功能与结构损伤。

Abstract

Objective

To investigate the effect of Tectoridin on myocardial injury post⁃myocardial infarction and its underlying mechanism.

Methods

By ligating the left anterior descending coronary artery in mice

we established a myocardial infarction mouse model. Cardiac function (left ventricular ejection fraction [EF] and fractional shortening [FS]) was assessed using small animal echocardiography

infarct size was quantified by TTC staining

GR1 neutrophil infiltration was detected via immunofluorescence

mRNA expression of inflammatory factors （IL⁃6

TNF⁃α

and IL⁃1β） was analyzed by RT⁃qPCR

and protein levels of apoptotic markers （Bax and Bcl2） and antioxidant proteins （Sod2

Nrf2

and Ho⁃1） were measured via Western Blot. The target specificity was validated using an Nrf2 knockout mouse model.

Results

Tectoridin significantly improved cardiac function after myocardial infarction （ejection fraction increased from 28.4% in the MI group to 38.5% in the Tectoridin group

0.01）

reduced infarct size by approximately 21%

suppressed neutrophil infiltration and inflammatory factor expression

and upregulated antioxidant proteins Sod2

Nrf2

and Ho⁃1. Mechanistically

Tectoridin activated the antioxidant pathway by promoting Nrf2 nuclear translocation

thereby reducing reactive oxygen species accumulation and cellular apoptosis

as evidenced by a decreased Bax/Bcl2 ratio. The cardioprotective effects of Tectoridin were abolished in Nrf2⁃knockout mice

confirming Nrf2 as its critical molecular target.

Conclusion

Tectoridin ameliorates cardiac function and structural damage after myocardial infarction by activating the Nrf2/Ho⁃1 pathway

thereby attenuating oxidative stress

inflammation

and apoptosis.

关键词

Keywords

references

CHONG B , JAYABASKARAN J , JAUHARI S M , et al . Global burden of cardiovascular diseases: Projections from 2025 to 2050 [J ] . Eur J Prev Cardiol , 2025 , 32 ( 11 ): 1001 ‑ 1015 .

ALLARA E , SHI W , BOLTON T , et al . Burden of cardiovascular diseases in England (2020–24): A national cohort using electronic health records data [J ] . Lancet Public Health , 2025 , 10 ( 11 ): e943 ‑ e954 .

NIJVELDT R , MAENG M , BEIJNINK C W H , et al . Immediate or deferred nonculprit‑lesion PCI in myocardial infarction [J ] . N Engl J Med , 2026 , 394 ( 10 ): 958 ‑ 968 .

UEYAMA H A , AKITA K , KIYOHARA Y , et al . Optimal strategy for complete revascularization in ST‑segment elevation myocardial infarction and multivessel disease a network meta‑analysis [J ] . J Am Coll Cardiol , 2025 , 85 ( 1 ): 19 ‑ 38 .

HAN X , ZHANG G Y , PANG M J , et al . Taohong Siwu decoction suppresses oxidative stress‑induced myocardial apoptosis post‑myocardial infarction by inhibiting PTEN pathway [J ] . Phytomedicine , 2024 , 135 : 155388 .

DUAN D P , LI H J , CHAI S Y , et al . The relationship between cardiac oxidative stress, inflammatory cytokine response, cardiac pump function, and prognosis post‑myocardial infarction [J ] . Sci Rep , 2024 , 14 : 8985 .

LIU X D , ZHANG W M , LUO J C , et al . TRIM21 deficiency protects against atrial inflammation and remodeling post myocardial infarction by attenuating oxidative stress [J ] . Redox Biol , 2023 , 62 : 102679 .

LIN Z J , HE H , CHEN P L , et al . Alpha‑ketoglutarate protects against myocardial infarction via FTO‑mediated anti‑inflammatory macrophage activation [J ] . Basic Res Cardiol , 2025 , 120 ( 5 ): 889 ‑ 912 .

HILGENDORF I , FRANTZ S , FRANGOGIANNIS N G . Repair of the infarcted heart: Cellular effectors, molecular mechanisms and therapeutic opportunities [J ] . Circ Res , 2024 , 134 ( 12 ): 1718 ‑ 1751 .

DHALLA N S , OSTADAL P , TAPPIA P S . Involvement of oxidative stress and antioxidants in modification of cardiac dysfunction due to ischemia–reperfusion injury [J ] . Antioxidants , 2025 , 14 ( 3 ): 11917 .

DONG H B , YOU Y W , YANG X L , et al . Total synthesis and anti‑inflammatory activity of tectoridin and related isoflavone glucosides [J ] . J Nat Prod , 2025 , 88 ( 1 ): 94 ‑ 102 .

WANG F S , KUO C W , KO J Y , et al . Irisin mitigates oxidative stress, chondrocyte dysfunction and osteoarthritis development through regulating mitochondrial integrity and autophagy [J ] . Antioxidants , 2020 , 9 ( 9 ): 810 .

LU T T , FENG Z , XUE H M , et al . Network pharmacology analysis and experimental validation of tectoridin in the treatment of ischemic stroke by inhibiting apoptosis and regulating inflammation [J ] . Int J Mol Sci , 2025 , 26 ( 4 ): 1402 .

浏览量

下载量

CSCD

文章被引用时，请邮件提醒。

提交

工具集

关联资源

三叶苷通过激活Nrf2信号通路保护心肌梗死后心肌重构

游泳运动对小鼠心肌梗死的保护作用：基于AMPK/PGC⁃1α通路

还原型烟酰胺腺嘌呤二核苷酸磷酸氧化酶2在阿霉素诱导的小鼠心肌损伤中的作用

高通量测序临床报告中遗传变异正交实验验证的规范化建议

ICU严重多发伤并发急性呼吸窘迫综合征的危险因素分析