Reactive Oxygen Species in Myocardial Reperfusion Injury: From Physiopathology to Therapeutic Approaches

Cell death is an important component of the pathophysiology of any disease. Myocardial disease is no exception. Understanding how and why cells die, particularly in the heart where cardiomyocyte regeneration is limited at best, becomes a critical area of study. Ferroptosis is a recently described form of nonapoptotic cell death. It is an iron-mediated form of cell death that occurs because of accumulation of lipid peroxidation products. Reactive oxygen species and iron-mediated phospholipid peroxidation is a hallmark of ferroptosis. To date, ferroptosis has been shown to be involved in cell death associated with Alzheimer’s disease, Huntington’s disease, cancer, Parkinson’s disease, and kidney degradation. Myocardial reperfusion injury is characterized by iron deposition as well as reactive oxygen species production. These conditions, therefore, favor the induction of ferroptosis. Currently there is no available treatment for reperfusion injury, which accounts for up to 50% of the final infarct size. This review will summarize the evidence that ferroptosis can induce cardiomyocyte death following reperfusion injury and the potential for this knowledge to open new therapeutic approaches for myocardial ischemia-reperfusion injury.

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Pengaruh Lidokain Intravena Terhadap Kadar Superoxide Dismutase 1 (Sod-1) Paru Kelinci Dengan Lung Ischemic Reperfusion Injury Model

JAI (Jurnal Anestesiologi Indonesia) ◽

10.14710/jai.v7i3.10807 ◽

2015 ◽

Vol 7 (3) ◽

pp. 146

Author(s):

Mohammad Arief Kurniawan ◽

Johan Arifin ◽

Taufik Eko Nugroho

Keyword(s):

Reactive Oxygen Species ◽

Superoxide Dismutase ◽

Reperfusion Injury ◽

Reactive Oxygen ◽

Oxygen Species ◽

Superoxide Dismutase 1 ◽

Ischemic Reperfusion Injury ◽

Ischemic Reperfusion ◽

Injury Model

Latar belakang : Angka kejadian komplikasi paru paska operasi non jantung dibandingkan dengan komplikasi jantung yaitu 2,7% dan 2,5%. Penyebab hal ini adalah stres oksidatif, ketidakseimbangan radikal oksigen dan endogenous scavenging system.Lidokain menghambat saluran natrium dan, mengurangi masukan kalsium intraseluler, mengurangi produksi Reactive Oxygen Species (ROS) dan modulasi bioenergetika mitokondria, sehingga diharapkan lidokain mampu meningkatkan kadar antioksidan alami di dalam sel.Superoxide Dismutase-1 (SOD-1) adalah salah satu antioksidan alami didalam sel yang berperan dalam melindungi organ dari anion superoksida yang berbahaya dengan mengubah anion yang dihasilkan dari cedera setelah ischaemia-reperfusion.Tujuan : Mengetahui efek lidokain intravena terhadap kadar Superoxide Dismutase 1 (SOD-1) paru kelinci dengan lung ischemic reperfusion injury model.Metode : Desain eksperimental laboratorik, 16 kelinci dibagi menjadi dua kelompok secara acak. Kelompok kontrol mendapat perlakuan lung ischemic reperfusion injury dan kelompok perlakuan dilakukan lung ischemic reperfusion injurydan mendapat injeksi lidokain 1,5mg/kgBB/jam intravena secara kontinyu kemudian diukur kadar SOD-1 jaringan paru kedua kelompok. Uji normalitas menggunakan uji Shapiro Wilk dilanjutkan uji beda Independent T-test.Hasil : Kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injurydan mendapat lidokain lebih tinggi secara signifikan (p=0,01) dibandingkan dengan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injuryKesimpulan : Pemberian lidokain kontinyu intravena dapat meningkatkan kadar SOD-1 paru kelinci dengan lung ischemic reperfusion injury.

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