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

Oral carotenoids and polyphenols have been suggested to induce photo-protective effects. The aim of the study was to test whether the combination of carotenoids and polyphenols produce greater protective effects from UV-induced damage to skin cells. Such damage is characterized by inflammation and oxidative stress; thus, the photo-protective effect can be partially explained by modulating the nuclear factor kappa B (NFκB) and antioxidant response element/Nrf2 (ARE/Nrf2) transcription systems, known as important regulators of these two processes. Indeed, it was found in keratinocytes that carotenoids and polyphenols inhibit UVB-induced NFκB activity and release of cytokine IL-6. A combination of tomato extract with rosemary extract inhibited UVB-induced release of IL-6 more than each of the compounds alone. Moreover, this combination synergistically activated ARE/Nrf2 transcription systems. Inflammatory cytokines such as IL-6 and TNFα induce the expression of matrix metalloproteinases (MMPs), which leads to collagen breakdown; thus, it is important to note that carnosic acid reduced TNFα-induced MMP-1 secretion from human dermal fibroblasts. The in vitro results suggest beneficial effects of phytonutrient combinations on skin health. To assure that clinical experiments to prove such effects in humans are feasible, the human bioavailability of carotenoids from tomato extract was tested, and nearly a twofold increase in their plasma concentrations was detected. This study demonstrates that carotenoids and polyphenols cooperate in balancing UV-induced skin cell damage, and suggests that NFκB and ARE/Nrf2 are involved in these effects.

Download Full-text

Acute myocardial injury during cardiopulmonary bypass

American Heart Journal ◽

10.1016/0002-8703(58)90201-1 ◽

1958 ◽

Vol 56 (6) ◽

pp. 926-928 ◽

Cited By ~ 1

Author(s):

Robert S. Fraser ◽

Richard E. Rossall

Keyword(s):

Cardiopulmonary Bypass ◽

Myocardial Injury ◽

Acute Myocardial Injury

Download Full-text

Protective efficacy of carnosic acid against hydrogen peroxide induced oxidative injury in HepG2 cells through the SIRT1 pathway

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2014-0513 ◽

2015 ◽

Vol 93 (8) ◽

pp. 625-631 ◽

Cited By ~ 8

Author(s):

Yan Hu ◽

Ning Zhang ◽

Qing Fan ◽

Musen Lin ◽

Ce Zhang ◽

...

Keyword(s):

Hydrogen Peroxide ◽

Hepg2 Cells ◽

Manganese Superoxide Dismutase ◽

Caspase 3 ◽

Protective Efficacy ◽

B Cell Lymphoma ◽

Sirtuin 1 ◽

Carnosic Acid ◽

Protective Effects ◽

Hepatocyte Damage

Carnosic acid (CA), found in rosemary, has been reported to have antioxidant and antiadipogenic properties. Here, we investigate the molecular mechanism by which CA inhibits hydrogen peroxide (H2O2)-induced injury in HepG2 cells. Cells were pretreated with 2.5–10 μmol/L CA for 2 h and then exposed to 3 mmol/L H2O2 for an additional 4 h. CA dose-dependently increased cell viability and decreased lactate dehydrogenase activities. Pretreatment with CA completely attenuated the inhibited expression of manganese superoxide dismutase (MnSOD) and the B-cell lymphoma-extra large (Bcl-xL), and reduced glutathione activity caused by H2O2, whereas it reversed reactive oxygen species accumulation and the increase in cleaved caspase-3. Importantly, sirtuin 1 (SIRT1), a NAD+-dependent deacetylase, was significantly increased by CA. Considering the above results, we hypothesized that SIRT1 may play important roles in the protective effects of CA in injury induced by H2O2. As expected, SIRT1 suppression by Ex527 (6-chloro-2,3,4,9-tetrahydro-1H-carbazole-1-carboxamide) and siRNA-mediated SIRT1 silencing (si-SIRT1) significantly aggravated the H2O2-induced increased level of cleaved caspase-3 but greatly reduced the decreased expression of MnSOD and Bcl-xL. Furthermore, the positive regulatory effect of CA was inhibited by si-SIRT1. Collectively, the present study indicated that CA can alleviate H2O2-induced hepatocyte damage through the SIRT1 pathway.

Download Full-text

Zingerone Alleviates Myocardial Ischemia/Reperfusion Injury

Current Topics in Nutraceutical Research ◽

10.37290/ctnr2641-452x.19:543-549 ◽

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.

Download Full-text

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

Download Full-text

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

Download Full-text

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.

Download Full-text

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.

Download Full-text