Tectoridin ameliorates myocardial injury after acute myocardial infarction through anti‐inflammatory and antioxidant stress mechanisms

FAN Haomiao; LI Yang; WANG Chenyang; ZHAO Yuhang; ZHOU Jianliang

doi:10.14188/j.1671-8852.2026.0011

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Tectoridin ameliorates myocardial injury after acute myocardial infarction through anti‐inflammatory and antioxidant stress mechanisms

更新时间：2026-11-05

- Tectoridin ameliorates myocardial injury after acute myocardial infarction through anti‐inflammatory and antioxidant stress mechanisms
- Medical Journal of Wuhan University Vol. 47, Issue 10, Pages: 1318-1324(2026)
- 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：
- 基金信息：
- DOI：10.14188/j.1671-8852.2026.0011
  CLC： R54
- Received：05 January 2026，
  
  Published：25 October 2026
- 稿件说明：
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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

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