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

2018 ◽  
Vol 120 (4) ◽  
pp. 5695-5703 ◽  
Author(s):  
Yang Liu ◽  
Yuanhang Liu ◽  
Xuecheng Huang ◽  
Jingchang Zhang ◽  
Lihui Yang
Keyword(s):  
Myocardial Injury ◽  
Protective Effects ◽  
Coronary Microembolization

Zingerone Alleviates Myocardial Ischemia/Reperfusion Injury

2021 ◽  
Vol 19 (4) ◽  
pp. 543-549
Author(s):  
Fanglin Luo ◽  
Shunxiang Luo ◽  
Yanqing Wu
Keyword(s):  
Myocardial Infarction ◽  
Proinflammatory Cytokine ◽  
Myocardial Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Underlying Mechanism ◽  
Protective Effects ◽  
Cytokine Release ◽  
Myocardial Ischemia Reperfusion Injury ◽  
Myocardial Ischemia Reperfusion

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.

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

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.

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

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.

scholarly journals Mechanism of Metformin on LPS-Induced Bacterial Myocarditis

Dose-Response ◽  
2019 ◽  
Vol 17 (2) ◽  
pp. 155932581984740 ◽  
Author(s):  
Minghua Li ◽  
Yawei Gou ◽  
Hongmei Yu ◽  
Tiefeng Ji ◽  
Yi Li ◽  
...  
Keyword(s):  
Myocardial Injury ◽  
Potential Role ◽  
Nuclear Factor ◽  
Protective Effects ◽  
H9c2 Cells ◽  
Expression Levels ◽  
Opposite Trend ◽  
Mitogen Activated Protein ◽  
Related Proteins

Aims: Metformin is commonly used to treat type 2 diabetes mellitus; however, in recent years, it was found to play a potential role in the protection of myocardial injury. In this study, we intended to investigate whether metformin had protective effects on bacterial myocarditis. Methods and Results: We stimulated rat cardiac myoblast H9c2 cells with lipopolysaccharide (LPS) and administrated with metformin. The results showed that cell viability after LPS stimulation was greatly reduced. The expression levels of phosphorylated p38 mitogen-activated protein kinases (MAPK) and c-Jun N-terminal kinases (JNK), nuclear factor (NF)-κB (NF-κB), BAX, and cleaved Caspase3 were significantly increased, while the expression of antiapoptotic protein Bcl-2 showed a prominent decrease compared to control. Nevertheless, the cells activity increased remarkably after metformin administration, and the expression levels of intracellular related proteins showed the opposite trend to that of the LPS group. Conclusion: We demonstrate that LPS stimulation may activate intracellular MAPK/JNK and NF-κB signaling pathways and thus induce cell apoptosis. In contrast, metformin reduced apoptosis by inhibiting this signaling pathway and increasing the expression level of Bcl-2. Moreover, it was found that metformin could enhance the ability of cells to antagonize redox damage by regulating the activities of superoxide dismutase and lactate dehydrogenase and subsequently promote the recovery of cardiomyocyte function.

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

2016 ◽  
Vol 31 (1) ◽  
pp. e21832 ◽  
Author(s):  
Mukesh Kumar ◽  
Eshvendar Reddy Kasala ◽  
Lakshmi Narendra Bodduluru ◽  
Vikas Kumar ◽  
Mangala Lahkar
Keyword(s):  
Myocardial Injury ◽  
Protective Effects ◽  
Biochemical Evidence ◽  
Acute Myocardial Injury

scholarly journals Modulatory Effect of Guinep (Melicoccus bijugatus Jacq) Fruit Pulp Extract on Isoproterenol-Induced Myocardial Damage in Rats. Identification of Major Metabolites Using High Resolution UHPLC Q-Orbitrap Mass Spectrometry

Molecules ◽  
2019 ◽  
Vol 24 (2) ◽  
pp. 235 ◽  
Author(s):  
Chukwuemeka Nwokocha ◽  
Isheba Warren ◽  
Javier Palacios ◽  
Mario Simirgiotis ◽  
Magdalene Nwokocha ◽  
...  
Keyword(s):  
Mass Spectrometry ◽  
High Resolution ◽  
Myocardial Injury ◽  
Weight Ratio ◽  
Mass Spectrometry Analysis ◽  
Control Group ◽  
Qtc Interval ◽  
Protective Effects ◽  
Orbitrap Mass Spectrometry ◽  
Hematological Analysis

Guinep is traditionally used in the management of cardiovascular ailments. This study aims to evaluate its medicinal constituents and effects in the management of myocardial injury in an experimental isoproterenol (ISO) rat model. Sprague-Dawley rats were randomly assigned to four groups: Group 1 was the control group; Group 2 received M. bijugatus extract (100 mg/Kg; MB) for six weeks; Group 3 was given ISO (85 mg/Kg) i.p. twice during a 24-hour period; and Group 4 was given ISO (85 mg/Kg) i.p. and MB extract (100 mg/Kg) for six weeks. The MB was administered orally by gavage, daily. The blood pressure of conscious animals was measured, while ECG was performed under anesthesia. Blood and serum were collected for biochemical and hematological analysis. The ISO group treated with MB showed a significant decrease (p < 0.001) in (SBP), diastolic (DBP), mean arterial (MAP) and heart rate (HR) compared to the ISO only group. Conversely, MB treated rats that were not induced with ISO displayed a significant decreases (p < 0.001) in SBP, DBP, MAP, and HR. ISO significantly elevated the ST segment (p < 0.001) and shortened the QTc interval (p < 0.05), which were recovered after treatment with 100 mg/Kg of MB. In addition, the results showed a significant decrease (p < 0.001) in the heart to body weight ratio of the ISO group treated with MB compared to the ISO only group. Furthermore, the extract normalized the hematological values depressed by the ISO while significantly elevating the platelet count. UHPLC high-resolution orbitrap mass spectrometry analysis results revealed the presence of several antioxidants like vitamin C and related compounds, phenolic acids, flavonoid, fatty acids (oxylipins), and terpene derivatives. The results of this study indicated that Melicoccus bijugatus did display some cardio-protective effects in relation to myocardial injury.

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