Key Takeaways & Executive Findings
- •• Artemisinin significantly improves myocardial blood perfusion in arsenic-poisoned rats, as evidenced by increased AUC and WIS×PI values on myocardial contrast echocardiography. • Artemisinin reduces arsenic-induced myocardial microvascular damage and inflammation, indicated by decreased CD31 expression and restored myocardial ultrastructure. • The protective effects of artemisinin are dose-dependent, with high-dose (60 mg/kg) showing greater efficacy than low-dose (30 mg/kg). • This study provides a potential therapeutic strategy for arsenic-induced cardiotoxicity, highlighting artemisinin's dual antioxidant and anti-inflammatory actions.
Abstract
Arsenic is widely present in nature, and its compounds are extensively used in industrial, agricultural, and medical fields. Arsenic trioxide (As2O3) is specifically used as a therapeutic agent for acute promyelocytic leukemia because it induces cancer cell differentiation and apoptosis, significantly reduces the cancer cell count and has unique medical value. However, owing to its high toxicity and carcinogenicity, long-term use can induce cardiovascular diseases such as arrhythmia and myocardial contractile dysfunction. However, research on the treatment of arsenic-induced cardiotoxicity remains relatively scarce. Notably, artemisinin has anti-inflammatory and antioxidative effects on various heart diseases, effectively inhibiting reactive oxygen species (ROS) production, preventing myocardial damage and apoptosis caused by arsenic poisoning, and improving cardiac contractile and diastolic functions, thus enhancing cardiac function. This study aims to discuss the impact of artemisinin on the myocardium of arsenic-poisoned rats. Forty 12-week-old male SD rats were randomly divided into five groups: control, arsenic poisoning, drug control, low-dose artemisinin, and high-dose artemisinin. As2O3 was intraperitoneally injected at 5 mg/kg/day for 10 days in the arsenic poisoning, low-dose, and high-dose groups, whereas the control and drug control groups received equal volumes of physiological saline. Artemisinin was subsequently injected at corresponding doses for three weeks. Myocardial contrast echocardiography (MCE) was used to assess myocardial blood perfusion. Blood and myocardial tissue samples were collected for biochemical and histological analyses. Results showed that arsenic poisoning significantly decreased myocardial blood perfusion (AUC and WIS×PI) and increased CD31 expression, indicating microvascular damage and inflammation. Artemisinin intervention, especially at high dose, restored perfusion and reduced CD31 expression, suggesting a protective effect. Electron microscopy confirmed that artemisinin alleviated arsenic-induced myocardial structural damage. These findings suggest that artemisinin alleviates arsenic-induced myocardial injury by modulating oxidative stress and inflammatory responses.
1. Introduction
Arsenic is widely present in nature, and its compounds are extensively used in industrial, agricultural, and medical fields [1]. Arsenic trioxide (As2O3) is specifically used as a therapeutic agent for acute promyelocytic leukemia because it induces cancer cell differentiation and apoptosis, significantly reduces the cancer cell count and has unique medical value [2]. However, owing to its high toxicity and carcinogenicity, long-term use can induce cardiovascular diseases such as arrhythmia and myocardial contractile dysfunction [3].
However, research on the treatment of arsenic-induced cardiotoxicity remains relatively scarce. Notably, artemisinin has anti-inflammatory and antioxidative effects on various heart diseases, effectively inhibiting reactive oxygen species (ROS) production, preventing myocardial damage and apoptosis caused by arsenic poisoning, and improving cardiac contractile and diastolic functions, thus enhancing cardiac function [4]. This study aims to discuss the impact of artemisinin on the myocardium of arsenic-poisoned rats.
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Wenjuan Qin, Yifei Zhou, Chuncui Chen, Xueting Guo, Ruimeng Tian, Ruoxi Chen, Wenrong Shi, Lei Huang, Caiyun Zhang, Shanshan Dong, Guilin Lu (2026). Artemisinin alleviates arsenic-induced myocardial injury in rats by modulating oxidative stress and inflammatory responses. Acta Biochimica et Biophysica Sinica. https://doi.org/10.3724/abbs.2024225
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Frequently Asked Questions
What is the main finding of this study?
The study demonstrates that artemisinin alleviates arsenic-induced myocardial injury in rats by modulating oxidative stress and inflammatory responses, improving myocardial blood perfusion and reducing microvascular damage.
How was myocardial injury assessed in the rats?
Myocardial injury was assessed using myocardial contrast echocardiography (MCE) to measure blood perfusion parameters (AUC, WIS×PI), along with biochemical markers, CD31 immunofluorescence, and electron microscopy for structural analysis.
What doses of artemisinin were used in the study?
Two doses of artemisinin were used: a low dose of 30 mg/kg and a high dose of 60 mg/kg, administered for three weeks after arsenic exposure.
Why is artemisinin considered a potential treatment for arsenic-induced cardiotoxicity?
Artemisinin has known anti-inflammatory and antioxidant properties, which can counteract the oxidative stress and inflammation caused by arsenic, thereby protecting myocardial cells and improving cardiac function.
What are the clinical implications of this research?
This research suggests that artemisinin could be repurposed as a therapeutic agent to mitigate cardiotoxic side effects in patients undergoing arsenic trioxide treatment for acute promyelocytic leukemia, potentially improving their cardiac outcomes.
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