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Updated: Dec 28, 2025
Improved Rodent Model of Myocardial Ischemia and Reperfusion Injury
Published on: March 7, 2022
Attenuation of ROS-mediated myocardial ischemia-reperfusion injury by morin via regulation of RISK/SAPK pathways
Vipin Kumar Verma1, Salma Malik1, Ekta Mutneja1
1Cardiovascular Research Laboratory, Department of Pharmacology, All India Institute of Medical Sciences, New Delhi, 110029, India.
Background:
Oxidative stress plays an important role in the pathogenesis of myocardial ischemia-reperfusion (IR) injury. Morin, a bioflavonoid, has demonstrated antioxidant, anti-inflammatory and other diverse pharmacological activities in various experimental models such as isoproterenol-induced myocardial injury, doxorubicin-induced cardiotoxicity and neurotoxicity, as well as cisplatin-induced nephrotoxicity. Thus, this study aimed to evaluate the effect of morin in myocardial IR injury model and its underlying mechanisms.
Method:
To accomplish this, male albino Wistar rats were pre-treated with morin (40 and 80 mg/kg; po) for 28 days and on 29th day, rats experienced 45-min myocardial ischemia followed by 60-min reperfusion.
Results:
In comparison to IR-control group, morin pre-treatment significantly normalized hemodynamic parameters, restored antioxidant status, improved pathological changes, reduced the release of cardiac injury markers, inhibited inflammation (TNF-α/IL-6/NFκB/IKKβ) and apoptosis (increased Bcl-2, decreased Bax/Caspase-3 and TUNEL positivity) in the myocardium. This improvement in antioxidant, inflammation and anti-apoptosis markers could be due to downregulation of SAPK (p38/JNK) pathway and upregulation of survival kinase, i.e. RISK pathway (ERK/eNOS) in the myocardium.
Conclusion:
Thus, morin attenuated myocardial IR injury in rats by regulation of RISK/SAPK pathways.
Insights
Morin, a bioflavonoid, protects against heart damage from ischemia-reperfusion injury by reducing inflammation and apoptosis. It achieves this by modulating survival and stress-activated pathways in the heart.
Area of Science:
- Biochemistry
- Pharmacology
- Cardiology
Background:
- Oxidative stress is a key factor in myocardial ischemia-reperfusion (IR) injury.
- Morin, a bioflavonoid, exhibits antioxidant and anti-inflammatory properties.
- Previous studies show morin's protective effects in various organ toxicities.
Purpose of the Study:
- To investigate the protective effects of morin against myocardial IR injury.
- To elucidate the underlying molecular mechanisms of morin's action.
Main Methods:
- Male Wistar rats were pre-treated with morin (40 and 80 mg/kg) for 28 days.
- Myocardial IR injury was induced by 45 minutes of ischemia followed by 60 minutes of reperfusion.
- Hemodynamic parameters, cardiac markers, oxidative stress, inflammation, and apoptosis were assessed.
Main Results:
- Morin pre-treatment normalized hemodynamic parameters and improved cardiac function.
- Morin restored antioxidant status and reduced cardiac injury markers.
- Morin inhibited inflammation (TNF-α, IL-6, NFκB/IKKβ) and apoptosis (Bcl-2, Bax, Caspase-3, TUNEL).
- These effects were linked to the downregulation of the SAPK (p38/JNK) pathway and upregulation of the RISK (ERK/eNOS) pathway.
Conclusions:
- Morin effectively attenuates myocardial IR injury in a rat model.
- Morin exerts its protective effects through the regulation of RISK and SAPK signaling pathways.
