Related Experiment Video
Updated: Jul 31, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Mitochondrial dysfunction and cardiac ischemia/reperfusion injury are attenuated by nandrolone: Role of JAK-STAT3
Ainá E Domingos1, Fernando A C Seara2, Dahienne F Oliveira3
1Instituto de Biofísica Carlos Chagas Filho, Universidade Federal do Rio de Janeiro, Rio de Janeiro, Brazil.
Aim:
To investigate the effect of acute treatment with the anabolic steroid (AS) nandrolone decanoate in mitochondrial homeostasis and JAK-STAT3 signaling during the progression of cardiac ischemia/reperfusion injury (IR).
Methods:
Male Wistar rats (2 months old) were randomly allocated into four experimental groups: Control (CTRL), IR, AS, and AS + AG490. All animals were euthanized 3 days after a single intramuscular injection of nandrolone at 10 mg/kg (AS and AS + AG490 groups) or vehicle (CTRL and IR groups). Baseline mRNA expression of antioxidant enzymes superoxide dismutase (SOD) 1 and 2, glutathione peroxidase, catalase, and myosin heavy chain (MHC) α and β were compared between CTRL and AS groups. Isolated hearts were submitted to ex vivo ischemia and reperfusion, except for hearts from the CTRL group. Before the IR protocol, the JAK-STAT3 inhibitor AG490 was perfused in hearts from the AS + AG490 group. Heart samples were collected during reperfusion to investigate the effects on mitochondrial function. Results Antioxidant enzyme mRNA expression was unaffected, whereas the AS group exhibited decreased β- MHC/α-MHC ratio versus the CTRL group. Compared to the IR group, the AS group exhibited better recovery of post-ischemic left ventricular (LV) end-diastolic pressure and LV-developed pressure levels, while infarct size significantly decreased. Furthermore, mitochondrial production, transmembrane potential, and swelling were improved, whereas ROS formation was decreased versus the IR group. These effects were prevented by the perfusion of JAK-STAT3 inhibitor AG490.
Conclusion:
These findings suggest that acute nandrolone treatment can provide cardioprotection by recruiting the JAK-STAT3 signaling pathway and mitochondrial preservation.
Insights
Acute nandrolone treatment protects the heart from ischemia/reperfusion injury by preserving mitochondrial function and activating the JAK-STAT3 pathway. This anabolic steroid intervention improved cardiac recovery and reduced infarct size in a rat model.
Area of Science:
- Cardiovascular Research
- Mitochondrial Biology
- Pharmacology
Background:
- Cardiac ischemia/reperfusion (IR) injury is a major cause of heart damage.
- Mitochondrial dysfunction and JAK-STAT3 signaling play critical roles in IR injury progression.
- Anabolic steroids (AS) effects on cardiac IR injury are not fully understood.
Purpose of the Study:
- To investigate the cardioprotective effects of acute nandrolone decanoate treatment on mitochondrial homeostasis.
- To examine the role of JAK-STAT3 signaling in nandrolone-mediated cardioprotection during cardiac IR.
- To assess the impact of nandrolone on cardiac function and infarct size following IR.
Main Methods:
- Male Wistar rats were subjected to ex vivo cardiac ischemia/reperfusion.
- Animals received acute nandrolone decanoate treatment or vehicle.
- JAK-STAT3 signaling was inhibited using AG490.
- Mitochondrial function, oxidative stress, and cardiac performance were assessed.
Main Results:
- Nandrolone treatment improved post-ischemic cardiac function and reduced infarct size.
- Mitochondrial production, membrane potential, and swelling were favorably altered by nandrolone.
- Reactive oxygen species (ROS) formation was decreased following nandrolone administration.
- The cardioprotective effects of nandrolone were abolished by JAK-STAT3 inhibition.
Conclusions:
- Acute nandrolone decanoate administration confers significant cardioprotection against IR injury.
- The JAK-STAT3 signaling pathway is crucial for mediating nandrolone's beneficial effects.
- Nandrolone preserves mitochondrial homeostasis, contributing to its protective role in cardiac IR.
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