Oligomers of Resveratrol and Ferulic Acid Prepared by Peroxidase-Catalyzed Oxidation and Their Protective Effects on Cardiac Injury

2007 ◽  
Vol 55 (19) ◽  
pp. 7753-7757 ◽  
Author(s):  
Bei-Bei Yu ◽  
Xiu-Zhen Han ◽  
Hong-Xiang Lou
Keyword(s):  
Ferulic Acid ◽  
Cardiac Injury ◽  
Protective Effects ◽  
Catalyzed Oxidation

scholarly journals Protective effects of angiotensin-type1-receptor antagonism against isoproterenol (ISO)-induced cardiac injury in rats

1996 ◽  
Vol 27 (2) ◽  
pp. 259
Author(s):  
Daniela Grimm ◽  
Dietmar Eisner ◽  
Christina Peter ◽  
Günter Bruckschiegel ◽  
Günter A.J. Riegger ◽  
...  
Keyword(s):  
Cardiac Injury ◽  
Protective Effects ◽  
Receptor Antagonism

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 Comparison of the protective effects of steamed and cooked broccolis on ischaemia–reperfusion-induced cardiac injury

2009 ◽  
Vol 103 (6) ◽  
pp. 815-823 ◽  
Author(s):  
Subhendu Mukherjee ◽  
Istvan Lekli ◽  
Diptarka Ray ◽  
Hiranmoy Gangopadhyay ◽  
Utpal Raychaudhuri ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Cardiac Injury ◽  
Mitogen Activated Protein Kinase ◽  
Related Factor ◽  
Protective Effects ◽  
Extracellular Signal Regulated Kinase ◽  
Redox Signalling ◽  
Ischaemia Reperfusion ◽  
Extracellular Signal ◽  
Mitogen Activated Protein

Recently, broccoli, a vegetable of the Brassica family, has been found to protect the myocardium from ischaemic reperfusion injury through the redox signalling of sulphoraphane, which is being formed from glucosinolate present in this vegetable. Since cooked broccoli loses most of its glucosinolate, we assumed that fresh broccoli could be a superior cardioprotective agent compared to cooked broccoli. To test this, two groups of rats were fed with fresh (steamed) broccoli or cooked broccoli for 30 d, while a third group was given vehicle only for the same period of time. After 30 d, all the rats were sacrificed, and the isolated working hearts were subjected to 30 min ischaemia followed by 2 h of reperfusion. Both cooked and steamed broccolis displayed significantly improved post-ischaemic ventricular function and reduced myocardial infarction and cardiomyocyte apoptosis compared to control, but steamed broccoli showed superior cardioprotective abilities compared with the cooked broccoli. Corroborating with these results, both cooked and steamed broccolis demonstrated significantly enhanced induction of the survival signalling proteins including Bcl2, Akt, extracellular signal-regulated kinase 1/2, haemoxygenase-1, NFE2 related factor 2, superoxide dismutase (SOD1) and SOD2 and down-regulation of the proteins (e.g. Bax, c-Jun N-terminal kinase, p38 mitogen-activated protein kinase) of the death signalling pathway, steamed broccoli displaying superior results over its cooked counterpart. The expressions of proteins of the thioredoxin (Trx) superfamily including Trx1 and its precursor sulphoraphane, Trx2 and Trx reductase, were enhanced only in the steamed broccoli group. The results of the present study documented superior cardioprotective properties of the steamed broccoli over cooked broccoli because of the ability of fresh broccoli to perform redox signalling of Trx.

scholarly journals Piperine Alleviates Doxorubicin-Induced Cardiotoxicity via Activating PPAR-γ in Mice

PPAR Research ◽  
2019 ◽  
Vol 2019 ◽  
pp. 1-11 ◽  
Author(s):  
Jie Yan ◽  
Si-Chi Xu ◽  
Chun-Yan Kong ◽  
Xiao-Yang Zhou ◽  
Zhou-Yan Bian ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Injury ◽  
Inflammatory Factors ◽  
Peroxisome Proliferator ◽  
Protective Effects ◽  
Peroxisome Proliferator Activated Receptor ◽  
Ppar Γ ◽  
Myocardial Oxidative Stress

Background. Oxidative stress, inflammation and cardiac apoptosis were closely involved in doxorubicin (DOX)-induced cardiac injury. Piperine has been reported to suppress inflammatory response and pyroptosis in macrophages. However, whether piperine could protect the mice against DOX-related cardiac injury remain unclear. This study aimed to investigate whether piperine inhibited DOX-related cardiac injury in mice. Methods. To induce DOX-related acute cardiac injury, mice in DOX group were intraperitoneally injected with a single dose of DOX (15 mg/kg). To investigate the protective effects of piperine, mice were orally treated for 3 weeks with piperine (50 mg/kg, 18:00 every day) beginning two weeks before DOX injection. Results. Piperine treatment significantly alleviated DOX-induced cardiac injury, and improved cardiac function. Piperine also reduced myocardial oxidative stress, inflammation and apoptosis in mice with DOX injection. Piperine also improved cell viability, and reduced oxidative damage and inflammatory factors in cardiomyocytes. We also found that piperine activated peroxisome proliferator-activated receptor-γ (PPAR-γ), and the protective effects of piperine were abolished by the treatment of the PPAR-γ antagonist in vivo and in vitro. Conclusions. Piperine could suppress DOX-related cardiac injury via activation of PPAR-γ in mice.

scholarly journals Nicotinamide riboside promotes autolysosome clearance in preventing doxorubicin-induced cardiotoxicity

2019 ◽  
Vol 133 (13) ◽  
pp. 1505-1521 ◽  
Author(s):  
Dong Zheng ◽  
Yi Zhang ◽  
Ming Zheng ◽  
Ting Cao ◽  
Grace Wang ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Defense Mechanism ◽  
Myocardial Dysfunction ◽  
Cardiac Injury ◽  
Autophagic Flux ◽  
Protective Effects ◽  
Nicotinamide Riboside ◽  
And Oxidative Stress ◽  
Cultured Cardiomyocytes ◽  
Lysosomal Acidification

Abstract Doxorubicin (DOX) is widely used as a first-line chemotherapeutic drug for various malignancies. However, DOX causes severe cardiotoxicity, which limits its clinical uses. Oxidative stress is one of major contributors to DOX-induced cardiotoxicity. While autophagic flux serves as an important defense mechanism against oxidative stress in cardiomyocytes, recent studies have demonstrated that DOX induces the blockage of autophagic flux, which contributes to DOX cardiotoxicity. The present study investigated whether nicotinamide riboside (NR), a precursor of nicotinamide adenine dinucleotide (NAD)+, prevents DOX cardiotoxicity by improving autophagic flux. We report that administration of NR elevated NAD+ levels, and reduced cardiac injury and myocardial dysfunction in DOX-injected mice. These protective effects of NR were recapitulated in cultured cardiomyocytes upon DOX treatment. Mechanistically, NR prevented the blockage of autophagic flux, accumulation of autolysosomes, and oxidative stress in DOX-treated cardiomyocytes, the effects of which were associated with restoration of lysosomal acidification. Furthermore, inhibition of lysosomal acidification or SIRT1 abrogated these protective effects of NR during DOX-induced cardiotoxicity. Collectively, our study shows that NR enhances autolysosome clearance via the NAD+/SIRT1 signaling, thereby preventing DOX-triggered cardiotoxicity.

Contribution of ferulic acid, γ-oryzanol and tocotrienols to the cardiometabolic protective effects of rice bran

2017 ◽  
Vol 32 ◽  
pp. 58-71 ◽  
Author(s):  
Cristina Perez-Ternero ◽  
Maria Alvarez de Sotomayor ◽  
Maria Dolores Herrera
Keyword(s):  
Ferulic Acid ◽  
Rice Bran ◽  
Protective Effects
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