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Camphene as a Protective Agent in Myocardial Ischemia/Reperfusion Injury
Rodopi Stamatiou1, Maria Anagnostopoulou1, Konstantina Ioannidou-Kabouri1
1Laboratory of Animal Physiology, School of Biology, Aristotle University of Thessaloniki, 54124 Thessaloniki, Greece.
Insights
Camphene protects the heart from ischemia/reperfusion (I/R) injury by reducing oxidative stress and ferroptosis. This natural compound demonstrates therapeutic potential for mitigating heart damage following I/R events.
Area of Science:
- Cardiology
- Biochemistry
- Pharmacology
Background:
- Myocardial ischemia/reperfusion (I/R) injury is a major cause of heart failure and mortality globally.
- Camphene exhibits anti-inflammatory and hypolipidemic properties, but its cardioprotective effects against I/R injury were unknown.
Purpose of the Study:
- To evaluate the cardioprotective role of camphene against I/R injury.
- To elucidate the underlying mechanisms of camphene's action in the heart during I/R.
Main Methods:
- Adult rats were pretreated with camphene before ex vivo I/R induction.
- Infarct size (TTC staining) and cardiomyocyte injury (LDH release) were measured.
- Oxidative stress markers, mitochondrial content (CS activity), and ferroptosis indicators were assessed.
Main Results:
- Camphene pretreatment significantly reduced myocardial infarct size and cardiomyocyte death post-I/R.
- Camphene decreased oxidative stress, enhanced antioxidant defense mechanisms (Nrf2 pathway, CAT, MnSOD, GR), and increased mitochondrial content.
- Ferroptosis was attenuated, indicated by decreased GPx4 expression and lipid peroxidation.
Conclusions:
- Camphene confers significant cardioprotection against I/R injury.
- The protective effects are mediated by maintaining redox homeostasis and inhibiting ferroptosis.
- Camphene holds therapeutic promise for treating I/R-induced heart damage.
Abstract:
Myocardial ischemia/reperfusion injury (I/R) and the resulting heart failure is one of the main causes of mortality and morbidity worldwide. Camphene has been shown to have anti-inflammatory and hypolipidemic properties; however, its role in the protection of the heart from ischemia and reperfusion has not been investigated. The cardioprotective role of camphene and the mechanism that mediates its action against I/R injury was evaluated in the present study. A single dose of camphene was administered in adult rats prior to ex vivo I/R induction. Infarct size was measured using 2,3,5-triphenyltetrazolium chloride (TTC) staining and cardiomyocyte injury was assessed by determining the release of the enzyme lactate dehydrogenase (LDH). Camphene pretreatment provided significant protection reducing myocardial infarct size and cell death after I/R. The effect was correlated with the reduction in oxidative stress as evidenced by the determination of protein carbonylation, GSH/GSSG ratio, the increase in mitochondrial content as determined by CS activity, and the modulation of antioxidant defense mechanisms (expression of Nrf2 and target genes and activities of CAT, MnSOD, and GR). Furthermore, ferroptosis was decreased, as demonstrated by downregulation of GPx4 expression and reduction in lipid peroxidation. The results suggest that camphene can protect the heart against I/R injury by maintaining redox homeostasis and can hold therapeutic potential for mitigating the detrimental effects of I/R in the heart.
