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Updated: Dec 27, 2025
A Doxorubicin-Induced Murine Model of Dilated Cardiomyopathy In Vivo
Published on: May 16, 2020
Anti-interleukin-5-neutralizing antibody attenuates caradiac injury and cadiac dysfunction by aggravating the
Dan Xian1, Yingying Zhan1, Zicong Yang2
1Xishu County People's Hospital affiliated to Hubei Univerisity of Science and Technology, Nanning, 530021, China.
Abstract:
Previous studies have demonstrated that interleukins (ILs) are closely associated with doxorubicin (DOX)-induced cardiac injury. IL-5 is an important member of the IL family, and this study was performed to investigate whether IL-5 affects DOX-induced cardiac injury and its underlying mechanisms. The cardiac IL-5 expression was first detected and the results showed that cardiac IL-5 levels were significantly lower in DOX-treated mice, and IL-5 was mainly derived from cardiac macrophage (Mø). In addition, some DOX-treated mice received an injection of anti-IL-5-neutralizing antibody (nAb), and we found that treatment with a mouse anti-IL-5 nAb significantly upregulated the levels of myocardial injury markers, aggravated cardiac dysfunction, increased M1 macrophage (Mø1) and decreased M2 macrophage (Mø2) differentiation, and promoted apoptotic marker expression. Furthermore, the effect of mouse IL-5 nAb on DOX-induced Mø differentiation and its role on mouse cardiomyocyte (MCM) cells apoptosis were detected in vitro, and the results exhibited that mouse IL-5 nAb promoted Mø1 differentiation but inhibited Mø2 differentiation in vitro and alleviated apoptosis in MCM cells. Our results found a mouse anti-IL-5 nAb-aggravated DOX-induced cardiac injury and dysfunction by alleviating the inflammatory response and myocardial cell apoptosis.
Insights
Interleukin-5 (IL-5) deficiency exacerbates doxorubicin-induced heart injury by promoting inflammation and cardiomyocyte apoptosis. Neutralizing IL-5 worsens cardiac dysfunction and myocardial damage in mice.
Area of Science:
- Cardiology
- Immunology
- Molecular Biology
Background:
- Interleukins (ILs) are implicated in doxorubicin (DOX)-induced cardiac injury.
- Interleukin-5 (IL-5) is a key IL family member, but its specific role in DOX cardiotoxicity is unclear.
Purpose of the Study:
- To investigate the effect of IL-5 on doxorubicin-induced cardiac injury.
- To elucidate the underlying mechanisms of IL-5's action in cardiac injury.
Main Methods:
- Assessed cardiac IL-5 expression in DOX-treated mice.
- Administered anti-IL-5-neutralizing antibody (nAb) to DOX-treated mice.
- Evaluated myocardial injury markers, cardiac function, macrophage differentiation (M1/M2), and apoptosis in vivo and in vitro.
Main Results:
- Cardiac IL-5 levels were significantly reduced in DOX-treated mice, with IL-5 primarily sourced from cardiac macrophages.
- Anti-IL-5 nAb treatment aggravated DOX-induced cardiac injury, dysfunction, M1 macrophage polarization, and apoptosis.
- In vitro, anti-IL-5 nAb promoted M1 and inhibited M2 macrophage differentiation, while alleviating cardiomyocyte apoptosis.
Conclusions:
- IL-5 plays a protective role against DOX-induced cardiac injury.
- IL-5 deficiency or neutralization exacerbates cardiotoxicity by increasing inflammation and cardiomyocyte apoptosis.
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