Molecular and biochemical evidence on the protective effects of quercetin in isoproterenol-induced acute myocardial injury in rats

Using a rat model, we have explored the underlying mechanism of ischemia/reperfusion (I/R)-mediated myocardial infarction and assessed the protective potential of zingerone. The results show that zingerone exhibits not only the myocardial protective effect, but also antioxidative and anti-inflammatory effects by suppression of markers of oxidation and proinflammatory cytokine release. Zingerone promotes protective effects against I/R-induced myocardial infarction by regulating Nrf2/HO-1 and NF-κB signaling pathways. These findings provide novel insights into the effects of zingerone on the cardioprotective mechanism of myocardial injury after I/R and may open new avenues for myocardial infarction treatment.

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Acute Myocardial Injury in a 45-year-old Female: Hypereosinophilic Syndrome

Hong Kong Journal of Emergency Medicine ◽

10.1177/102490791302000111 ◽

2013 ◽

Vol 20 (1) ◽

pp. 60-62

Author(s):

WC Lin ◽

YM Weng ◽

YL Chan ◽

H Chang ◽

SL Huang ◽

...

Keyword(s):

Myocardial Injury ◽

Hypereosinophilic Syndrome ◽

Acute Myocardial Injury

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Protective effects and mechanism of curcumin on myocardial injury induced by coronary microembolization

Journal of Cellular Biochemistry ◽

10.1002/jcb.27854 ◽

2018 ◽

Vol 120 (4) ◽

pp. 5695-5703 ◽

Cited By ~ 2

Author(s):

Yang Liu ◽

Yuanhang Liu ◽

Xuecheng Huang ◽

Jingchang Zhang ◽

Lihui Yang

Keyword(s):

Myocardial Injury ◽

Protective Effects ◽

Coronary Microembolization

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Alpha-Lipoic Acid Protects Cardiomyocytes against Heat Stroke-Induced Apoptosis and Inflammatory Responses Associated with the Induction of Hsp70 and Activation of Autophagy

Mediators of Inflammation ◽

10.1155/2019/8187529 ◽

2019 ◽

Vol 2019 ◽

pp. 1-10

Author(s):

Hsin-Hsueh Shen ◽

Yu-Shiuan Tseng ◽

Ni-Chun Kuo ◽

Ching-Wen Kung ◽

Sherif Amin ◽

...

Keyword(s):

Lipoic Acid ◽

Myocardial Injury ◽

Inflammatory Responses ◽

Heat Stroke ◽

Heat Exposure ◽

Antioxidant Properties ◽

Mitochondrial Enzymes ◽

Protective Effects ◽

Anion Formation ◽

Anti Inflammatory

Heat stroke (HS) is a life-threatening illness and defined as when body temperature elevates above 40°C accompanied by the systemic inflammatory response syndrome that results in multiple organ dysfunctions. α-Lipoic acid (ALA) acts as a cofactor of mitochondrial enzymes and exerts anti-inflammatory and antioxidant properties in a variety of diseases. This study investigates the beneficial effects of ALA on myocardial injury and organ damage caused by experimental HS and further explores its underlying mechanism. Male Wistar rats were exposed to 42°C until their rectal core temperature reached 42.9°C and ALA was pretreared 40 or 80 mg/kg (i.v.) 1.5 h prior to heat exposure. Results showed that HS-induced lethality and hypothermia were significantly alleviated by ALA treatment that also improved plasma levels of CRE, LDH, and CPK and myocardial injury biomarkers myoglobin and troponin. In addition, ALA reduced cardiac superoxide anion formation and protein expression of cleaved caspase 3 caused by HS. Proinflammatory cytokine TNF-α and NF-κB pathways were significantly reduced by ALA treatment which may be associated with the upregulation of Hsp70. ALA significantly increased the Atg5-12 complex and LC3B II/LC3B I ratio, whereas the p62 and p-mTOR expression was attenuated in HS rats, indicating the activation of autophagy by ALA. In conclusion, ALA ameliorated the deleterious effects of HS by exerting antioxidative and anti-inflammatory capacities. Induction of Hsp70 and activation of autophagy contribute to the protective effects of ALA in HS-induced myocardial injury.

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Salidroside pretreatment protects against myocardial injury induced by heat stroke in mice

Journal of International Medical Research ◽

10.1177/0300060519868645 ◽

2019 ◽

Vol 47 (10) ◽

pp. 5229-5238

Author(s):

Guo-dong Chen ◽

Heng Fan ◽

Jian-Hua Zhu

Keyword(s):

Oxidative Stress ◽

Myocardial Injury ◽

Troponin I ◽

Heat Stroke ◽

Cardiac Injury ◽

Myocardial Damage ◽

Thiobarbituric Acid ◽

Protective Effects ◽

Creatine Kinase Mb ◽

Factor Α

Objective To explore the protective effects and mechanisms of salidroside on myocardial injury induced by heat stroke (HS) in mice. Methods We pretreated mice with salidroside for 1 week and then established an HS model by exposure to 41.2°C for 1 hour. We then examined the effects of salidroside on survival. We also assessed the severity of cardiac injury by pathology, and analyzed changes in levels of myocardial injury markers, inflammatory cytokines, and oxidative stress. Results Salidroside pretreatment significantly reduced HS-induced mortality and improved thermoregulatory function. Salidroside also provided significant protection against HS-induced myocardial damage, and decreased the expression levels of cardiac troponin I, creatine kinase-MB, and lactate dehydrogenase. Moreover, salidroside attenuated HS-induced changes in the inflammation markers tumor necrosis factor-α, interleukin (IL)-6, and IL-10, and down-regulated the oxidative stress response indicated by thiobarbituric acid reactant substances, malondialdehyde, reduced glutathione, and superoxide dismutase. Conclusions Salidroside pretreatment protected against HS-induced myocardial damage, potentially via a mechanism involving anti-inflammatory and anti-oxidative effects.

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