ArticleInternational journal of biological sciences2016
Carbon Monoxide Improves Neurologic Outcomes by Mitochondrial Biogenesis after Global Cerebral Ischemia Induced by Cardiac Arrest in Rats.
Article in International journal of biological sciences, 2016. The graph could read no effect estimate from its abstract, so it casts no vote on the map. Cited by 18 papers.
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Who cites it
18 citing papers in PubMed, 31 citations in OpenAlex.
- Therapeutic strategies to ameliorate mitochondrial oxidative stress in ischaemia-reperfusion injury: A narrative review.Clinical science (London, England : 1979) · 2025Review
- Neuroprotective Approaches for Brain Injury After Cardiac Arrest: Current Trends and Prospective Avenues.Journal of stroke · 2024Review
- Recent progress on anti-nociceptive effects of carbon monoxide releasing molecule-2 (CORM-2).Molecular and cellular biochemistry · 2024Review
- Carbon monoxide as a cellular protective agent in a swine model of cardiac arrest protocol.PloS one · 2024Article
- Neuroprotective Effect of miR-483-5p Against Cardiac Arrest-Induced Mitochondrial Dysfunction Mediated Through the TNFSF8/AMPK/JNK Signaling Pathway.Cellular and molecular neurobiology · 2023Article
- The role of (Diagnostic and interventional radiology (Ankara, Turkey) · 2023Article
- Mitochondrial Quality Control in Cerebral Ischemia-Reperfusion Injury.Molecular neurobiology · 2021Review
- Nature's marvels endowed in gaseous molecules I: Carbon monoxide and its physiological and therapeutic roles.Acta pharmaceutica Sinica. B · 2021Review
- Organic carbon monoxide prodrug, BW-CO-111, in protection against chemically-induced gastric mucosal damage.Acta pharmaceutica Sinica. B · 2021Article
- Short-term dietary restriction ameliorates brain injury after cardiac arrest by modulation of mitochondrial biogenesis and energy metabolism in rats.Annals of translational medicine · 2021Article
- Sodium-Glucose Co-Transporter 2 Inhibition With Empagliflozin Improves Cardiac Function After Cardiac Arrest in Rats by Enhancing Mitochondrial Energy Metabolism.Frontiers in pharmacology · 2021Article
- Making smart drugs smarter: The importance of linker chemistry in targeted drug delivery.Medicinal research reviews · 2020Review
- Rac1 relieves neuronal injury induced by oxygenglucose deprivation and re-oxygenation via regulation of mitochondrial biogenesis and function.Neural regeneration research · 2020Article
- Carbon monoxide: An emerging therapy for acute kidney injury.Medicinal research reviews · 2020Review
- PD98059 Protects Cerebral Cortex Mitochondrial Structure and Function at 48 h Post-Resuscitation in a Rat Model of Cardiac Arrest.Drug design, development and therapy · 2020Article
- Erythropoietin alleviates post-resuscitation myocardial dysfunction in rats potentially through increasing the expression of angiotensin II receptor type 2 in myocardial tissues.Molecular medicine reports · 2018Article
- An Overview of the Potential Therapeutic Applications of CO-Releasing Molecules.Bioinorganic chemistry and applications · 2018Review
- Devil or angel: two roles of carbon monoxide in stroke.Medical gas researchReview
Corrections and comments
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Authors and funding
13 authors at 2 institutions in 1 country.
Funding
No grant is acknowledged in the PubMed record.
Abstract
Mitochondrial dysfunction contributes to brain injury following global cerebral ischemia after cardiac arrest. Carbon monoxide treatment has shown potent cytoprotective effects in ischemia/reperfusion injury. This study aimed to investigate the effects of carbon monoxide-releasing molecules on brain mitochondrial dysfunction and brain injury following resuscitation after cardiac arrest in rats. A rat model of cardiac arrest was established by asphyxia. The animals were randomly divided into the following 3 groups: cardiac arrest and resuscitation group, cardiac arrest and resuscitation plus carbon monoxide intervention group, and sham control group (no cardiac arrest). After the return of spontaneous circulation, neurologic deficit scores (NDS) and S-100B levels were significantly decreased at 24, 48, and 72 h, but carbon monoxide treatment improved the NDS and S-100B levels at 24 h and the 3-day survival rates of the rats. This treatment also decreased the number of damaged neurons in the hippocampus CA1 area and increased the brain mitochondrial activity. In addition, it increased mitochondrial biogenesis by increasing the expression of biogenesis factors including peroxisome proliferator-activated receptor-γ coactivator-1α, nuclear respiratory factor-1, nuclear respiratory factor-2 and mitochondrial transcription factor A. Thus, this study showed that carbon monoxide treatment alleviated brain injury after cardiac arrest in rats by increased brain mitochondrial biogenesis.
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