Related Experiment Video
Updated: Mar 3, 2026

Protection of H9c2 Myocardial Cells from Oxidative Stress by Crocetin via PINK1/Parkin Pathway-Mediated Mitophagy
Published on: May 26, 2023
Carnosic acid protects against mitochondrial dysfunction and ferroptosis in myocardial ischemia/reperfusion injury
Xiu-Qi Wang1, Fa-Jia Hu1, Huang Huang2
1Department of Cardiovascular Surgery, The Second Affiliated Hospital, Jiangxi Medical College, Nanchang University, Nanchang, 330006, Jiangxi, China.
Abstract:
The pathogenesis of myocardial ischemia/reperfusion injury (MIRI) is complicated and involves various factors, including iron overload, oxidative stress, mitochondrial damage, calcium overload, and inflammation. Hence, the aim of this study was to explore the molecular mechanisms of MIRI and verify the myocardial protection mechanism of carnosic acid (CA) in MIRI. In vivo and in vitro MIRI models were established. The results of this study verified that pretreatment with CA effectively increased cell viability, reduced the apoptosis rate and lactate dehydrogenase activity, maintained mitochondrial dynamic balance, and inhibited iron overload and abnormal lipid metabolism in cardiomyocytes with anoxia/reoxygenation treatment. Pretreatment with CA not only improved cardiac function and reduced infarct size in rats treated with ischemia/reperfusion (I/R) but also decreased reactive oxygen species levels and the rate of apoptotic cardiomyocytes in myocardium induced by I/R. These cardioprotective effects of CA could be inhibited by treatment with adenoviral vector expressing Mfn2 short hairpin RNA. In general, CA pretreatment protected cardiomyocytes against MIRI injury by inhibiting ferroptosis and maintaining mitochondrial dynamic homeostasis through an Mfn2-dependent mechanism.
Insights
Carnosic acid (CA) protects heart cells from injury caused by blood flow interruption and restoration. It works by reducing cell death and maintaining mitochondrial health, particularly through a mechanism involving Mfn2.
Area of Science:
- Cardiology
- Molecular Biology
- Biochemistry
Background:
- Myocardial ischemia/reperfusion injury (MIRI) involves complex factors like iron overload, oxidative stress, and inflammation.
- Understanding MIRI's molecular mechanisms is crucial for developing effective treatments.
Purpose of the Study:
- To investigate the molecular mechanisms underlying MIRI.
- To evaluate the cardioprotective effects of carnosic acid (CA) against MIRI.
Main Methods:
- Established in vivo and in vitro models of MIRI.
- Assessed cell viability, apoptosis, lactate dehydrogenase activity, and mitochondrial dynamics.
- Investigated the role of Mfn2 in CA's protective effects using adenoviral vectors.
Main Results:
- CA pretreatment enhanced cardiomyocyte viability and reduced apoptosis and LDH activity.
- CA inhibited iron overload and abnormal lipid metabolism in anoxic/reoxygenated cardiomyocytes.
- CA improved cardiac function, reduced infarct size, and decreased oxidative stress and cardiomyocyte apoptosis in MIRI rats.
- CA's cardioprotective effects were dependent on Mfn2 expression.
Conclusions:
- CA protects cardiomyocytes against MIRI by inhibiting ferroptosis.
- CA maintains mitochondrial dynamic homeostasis via an Mfn2-dependent pathway.
- CA demonstrates significant therapeutic potential for treating MIRI.
More Related Videos
Related Concept Videos
Electron Transport Chain: Complex I and II
ROS generation is regulated and maintained at moderate levels necessary...
Necrosis
Morphological Manifestations of Necrosis
Necrotic cells show different types of morphological appearance depending on the type of tissue and infection. In coagulative necrosis, cells become...
Translocation of Proteins into the Mitochondria
Sorting of outer membrane proteins:
Mitochondrial outer membrane proteins are of two types: the transmembrane, beta-barrel porins, and the membrane-anchored, alpha-helical proteins. Beta-barrel porin precursors are translocated by the TOM complex and inserted into the outer mitochondrial membrane by the SAM complex. In contrast,...
Mitochondrial Precursor Proteins
Most of the mitochondrial...
Mitochondrial Membranes
Mitochondria

