scholarly journals Role of Platelet Activation and Oxidative Stress in the Evolution of Myocardial Infarction

2019 ◽  
Vol 24 (6) ◽  
pp. 509-520 ◽  
Author(s):  
Eduardo Fuentes ◽  
Rodrigo Moore-Carrasco ◽  
Antonio Marcus de Andrade Paes ◽  
Andres Trostchansky
Keyword(s):  
Oxidative Stress ◽  
Myocardial Infarction ◽  
Reperfusion Injury ◽  
Antiplatelet Therapy ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Coronary Thrombosis ◽  
Ischemia Reperfusion ◽  
Critical Role

Myocardial infarction, commonly known as heart attack, evolves from the rupture of unstable atherosclerotic plaques to coronary thrombosis and myocardial ischemia–reperfusion injury. A body of evidence supports a close relationship between the alterations following an ischemia–reperfusion injury-induced oxidative stress and platelet activity. Through their critical role in thrombogenesis and inflammatory responses, platelets are fully (totally) implicated from atherothrombotic plaque formation to myocardial infarction onset and expansion. However, mere platelet aggregation prevention does not offer full protection, suggesting that other antiplatelet therapy mechanisms may also be involved. Thus, the present review discusses the integrative role of platelets, oxidative stress, and antiplatelet therapy in triggering myocardial infarction pathophysiology.

Critical role of reactive nitrogen species in lung ischemia–reperfusion injury

2003 ◽  
Vol 22 (7) ◽  
pp. 784-793 ◽  
Author(s):  
Babu V Naidu ◽  
Charles Fraga ◽  
Andrew L Salzman ◽  
Csaba Szabo ◽  
Edward D Verrier ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Reactive Nitrogen Species ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Reactive Nitrogen ◽  
Nitrogen Species

Src protein tyrosine kinase family and acute inflammatory responses

2006 ◽  
Vol 291 (2) ◽  
pp. L129-L141 ◽  
Author(s):  
Daisuke Okutani ◽  
Monika Lodyga ◽  
Bing Han ◽  
Mingyao Liu
Keyword(s):  
Acute Lung Injury ◽  
Lung Injury ◽  
Tyrosine Kinase ◽  
Reperfusion Injury ◽  
Protein Tyrosine Kinase ◽  
Inflammatory Responses ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Protein Tyrosine

Acute inflammatory responses are one of the major underlying mechanisms for tissue damage of multiple diseases, such as ischemia-reperfusion injury, sepsis, and acute lung injury. By use of cellular and molecular approaches and transgenic animals, Src protein tyrosine kinase (PTK) family members have been identified to be essential for the recruitment and activation of monocytes, macrophages, neutrophils, and other immune cells. Src PTKs also play a critical role in the regulation of vascular permeability and inflammatory responses in tissue cells. Importantly, animal studies have demonstrated that small chemical inhibitors for Src PTKs attenuate tissue injury and improve survival from a variety of pathological conditions related to acute inflammatory responses. Further investigation may lead to the clinical application of these inhibitors as drugs for ischemia-reperfusion injury (such as stroke and myocardial infarction), sepsis, acute lung injury, and multiple organ dysfunction syndrome.

scholarly journals Critical role of acidic sphingomyelinase in murine hepatic ischemia-reperfusion injury

Hepatology ◽  
2006 ◽  
Vol 44 (3) ◽  
pp. 561-572 ◽  
Author(s):  
Laura Llacuna ◽  
Montserrat Marí ◽  
Carmen Garcia-Ruiz ◽  
José C. Fernandez-Checa ◽  
Albert Morales
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Hepatic Ischemia ◽  
Hepatic Ischemia Reperfusion

scholarly journals Neuroprotective effect of a new free radical scavenger HL-008 against ischemia-reperfusion injury

2020 ◽  
Author(s):  
Yahong Liu ◽  
Ying Cheng ◽  
Wei Zhang ◽  
Hongqi Tian
Keyword(s):  
Oxidative Stress ◽  
Reperfusion Injury ◽  
Brain Tissue ◽  
Cell Activation ◽  
Ischemia Reperfusion Injury ◽  
Neuroprotective Effect ◽  
Ischemia Reperfusion ◽  
Critical Role ◽  
Radical Scavenger

Abstract Oxidative stress plays a critical role in cerebral ischemia-reperfusion injury. We previously developed a powerful antioxidant, HL-008, and this study aimed to investigate the neuroprotective function of HL-008. The in vitro and in vivo efficacy of HL-008 was evaluated using a PC-12 cell oxidative stress model induced by hydrogen peroxide and a rat model of middle cerebral artery occlusion, respectively. The MTT assay was used to analyze cell viability. TTC staining, HE staining, immunofluorescence, western blot, and proteomics were used to evaluate the infarction volume, brain tissue morphology, apoptosis, inflammation, and related pathways. Indicators related to oxidative levels were mainly detected using commercial kits. HL-008 significantly reduced the cerebral infarction area induced by ischemia-reperfusion, improved the neurological score, alleviated oxidative stress and inflammation in the brain tissue, reduced glial cell activation, inhibited brain tissue apoptosis by influencing multiple signaling pathways, and had a neuroprotective effect. If HL-008 is successfully developed, it can significantly improve the quality of life of stroke patients.

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