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.

Protective Effect of Taraxasterol Against Myocardial Damage Caused by Sepsis Through Inhibition of Toll-Like Receptor 4/Nuclear Factor-Kappa B Signaling Pathway

2021 ◽  
Vol 19 (3) ◽  
pp. 339-344
Author(s):  
Shuquan Wang ◽  
Xuhui Tang
Keyword(s):  
Signaling Pathway ◽  
Troponin I ◽  
Morphological Changes ◽  
Cardiac Injury ◽  
Cecal Ligation ◽  
Myocardial Damage ◽  
Protective Effects ◽  
Toll Like Receptor 4 ◽  
Membrane Rupture ◽  
Creatine Kinase Mb

Taraxasterol exerts protective effects against vascular or neuroinflammation and hepatic injury. However, its role on myocardial damage caused by sepsis has not been thoroughly investigated. Myocardial tissues of septic rats - established by cecal ligation and puncture - show a disordered myocardial fiber arrangement, edema, nuclear membrane rupture, and inflammatory cell infiltration. Administration of taraxasterol to these rats attenuated the morphological changes in the myocardial tissues. Biomarkers of cardiac injury in sepsis such as cardiac troponin I, creatine kinase-MB, and lactic acid dehydrogenase were elevated in the plasma of septic rats, and the administration of taraxasterol decreased the rise in these biomarkers. Also, taraxasterol attenuated increase in the levels of inflammatory cytokines in myocardial tissues of septic rats. Based on the evaluation of changes in the mediators of TLR4/NF-κB signaling pathway in sepsis and following treatment with taraxasterol led us to conclude that taraxasterol alleviates myocardial damage in septic rats through inhibition of the TLR4/NF-κB signaling pathway.

scholarly journals Protective effects of bisoprolol against cadmium-induced myocardial toxicity through inhibition of oxidative stress and NF-κΒ signalling in rats

2021 ◽  
Vol 0 (0) ◽  
Author(s):  
Jinhua Liu ◽  
Ying Xie ◽  
Zhujun Han ◽  
Hailong Wang ◽  
Wenhu Xu
Keyword(s):  
Oxidative Stress ◽  
Cardiac Injury ◽  
Therapeutic Drug ◽  
Control Group ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Tissue Samples ◽  
Gum Acacia ◽  
Tnf Α ◽  
Creatine Kinase Mb

Abstract Introduction The aim of the study was to investigate the mitigative effects of bisoprolol (BIS) in cadmium-induced myocardial toxicity on oxidative stress and its inhibitive effect on nuclear factor kappa-light-chain-enhancer of activated B cells (NF-kB) signalling in rats. Material and Methods Male albino Wistar rats were assigned to control, Cd, BIS 2 (2 mg/kg b.w.) and BIS 8 (8 mg/kg b.w.) groups with nine rats in each. Over four weeks, the control group was administered 1% gum acacia, all other groups received 3mg/kg b.w. CdCl2 dissolved in distilled water, and the BIS groups were additionally given bisoprolol in gum acacia. Blood samples were collected for biochemical estimations. Blood pressure and serum biomarker (lactate dehydrogenase, aspirate transaminase, alanine transferase and creatine kinase-MB, enzyme (superoxide dismutase, lipid hydroxy peroxidase, catalase and malondialdehyde), and tumour necrosis factor alpha (TNF-α) concentrations were measured. Western blot analysis was conducted for NF-κB and glutathione S-transferase (GST). After sacrificing the rats, cardiac tissue samples were examined histopathologically. Results Our findings pointed to a significant decrease (P < 0.05) in the studied serum biomarkers and levels of the relevant enzymes in the BIS 8 group compared to the Cd group. A significant decrease (P < 0.05) in NF-kB p65 expression and TNF-α levels was noted in the BIS 8 group relative to the BIS 2 and Cd groups, indicating a reduction at a higher dose. In microscopy, histopathological changes in the cardiac muscles of the BIS 8 group were evident compared to those of the Cd group. Conclusion BIS seemed to have protective effects against cardiac injury induced by cadmium and could be considered a novel therapeutic drug and prognostic biomarker in the pathology of the many cardiovascular diseases caused by heavy metal intake.

scholarly journals Tempol, a Membrane-Permeable Radical Scavenger, Exhibits Anti-Inflammatory and Cardioprotective Effects in the Cerulein-Induced Pancreatitis Rat Model

2016 ◽  
Vol 2016 ◽  
pp. 1-7 ◽  
Author(s):  
Andrzej Marciniak ◽  
Beata Walczyna ◽  
Grażyna Rajtar ◽  
Sebastian Marciniak ◽  
Andrzej Wojtak ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Morphological Evidence ◽  
Radical Scavenger ◽  
Protective Effects ◽  
Cardiac Damage ◽  
Stress Changes ◽  
Sh Group ◽  
Long Time

To date, it remains unclear whether mild form of acute pancreatitis (AP) may cause myocardial damage which may be asymptomatic for a long time. Pathogenesis of AP-related cardiac injury may be attributed in part to ROS/RNS overproduction. The aim of the present study was to evaluate the oxidative stress changes in both the pancreas and the heart and to estimate the protective effects of 1-oxyl-2,2,6,6-tetramethyl-4-hydroxypiperidine (tempol) at the early phase of AP. Cerulein-induced AP led to the development of acute edematous pancreatitis with a significant decrease in the level of sulfhydryl (–SH) groups (oxidation marker) both in heart and in pancreatic tissues as well as a substantial increase in plasma creatine kinase isoenzyme (CK-MB) activity (marker of the heart muscle lesion) which confirmed the role of oxidative stress in the pathogenesis of cardiac damage. The tempol treatment significantly reduced the intensity of inflammation and oxidative damage and decreased the morphological evidence of pancreas injury at early AP stages. Moreover, it markedly attenuated AP-induced cardiac damage revealed by normalization of the –SH group levels and CK-MB activity. On the basis of these studies, it is possible to conclude that tempol has a profound protective effect against cardiac and pancreatic damage induced by AP.

scholarly journals The effect of short-term coenzyme Q10supplementation and pre-cooling strategy on cardiac damage markers in elite swimmers

2018 ◽  
Vol 119 (4) ◽  
pp. 381-390 ◽  
Author(s):  
Ali Emami ◽  
Asghar Tofighi ◽  
Siamak Asri-Rezaei ◽  
Behnaz Bazargani-Gilani
Keyword(s):  
Oxidative Stress ◽  
Troponin I ◽  
Coenzyme Q ◽  
Myocardial Damage ◽  
Cardiac Damage ◽  
Cooling Strategy ◽  
Creatine Kinase Mb ◽  
Elite Swimmers ◽  
Two Stages ◽  
And Control

AbstractStrenuous physical exercise and hyperthermia may paradoxically induce oxidative stress and adverse effects on myocardial function. The purpose of this study was to investigate the effect of 14-d coenzyme Q10(CoQ10) supplementation and pre-cooling on serum creatine kinase-MB (CK-MB), cardiac Troponin I (cTnI), myoglobin (Mb), lactate dehydrogenase (LD), total antioxidant capacity (TAC), lipid peroxidation (LPO) and CoQ10concentration in elite swimmers. In total, thirty-six healthy males (mean age 17 (sd1) years) were randomly selected and divided into four groups of supplementation, supplementation with pre-cooling, pre-cooling and control. During an eighteen-session protocol in the morning and evening, subjects attended speed and endurance swimming training sessions for 5 km in each session. Blood sampling was done before (two stages) and after (two stages) administration of CoQ10and pre-cooling. ANCOVA and repeated measurement tests with Bonferronipost hoctest were used for the statistical analysis of the data. There was no significant statistical difference among groups for the levels of CK-MB, cTnI, Mb, LD, TAC, LPO and CoQ10at the presampling (stages 1 and 2) (P>0·05). However, pre-cooling and control groups show a significant increase in the levels of CK-MB, cTnI, Mb, LD and LPO compared with the supplementation and supplementation with pre-cooling groups in the post-sampling (stages 1 and 2) (P<0·05), except for the TAC and CoQ10. Consequently, CoQ10supplementation prevents adverse changes of myocardial damage and oxidative stress during swimming competition phase. Meanwhile, the pre-cooling strategy individually has no desired effect on the levels of CK-MB, cTnI, Mb, LD, LPO, TAC and CoQ10.

scholarly journals Comparative sensitivity of cardiac troponin I and lactate dehydrogenase isoenzymes for diagnosing acute myocardial infarction

1996 ◽  
Vol 42 (11) ◽  
pp. 1770-1776 ◽  
Author(s):  
A S Jaffe ◽  
Y Landt ◽  
C A Parvin ◽  
D R Abendschein ◽  
E M Geltman ◽  
...  
Keyword(s):  
Myocardial Infarction ◽  
Acute Myocardial Infarction ◽  
Lactate Dehydrogenase ◽  
Cardiac Troponin ◽  
Troponin I ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Cardiac Troponin I ◽  
Retrospective Diagnosis ◽  
Creatine Kinase Mb

Abstract Criteria for the retrospective diagnosis of acute myocardial infarction rely heavily on increases in lactate dehydrogenase (LD) isoenzymes. However, increases of LD isoenzyme activities are not specific for myocardial injury. Recently, increased concentrations of cardiac troponin I (cTnI) have been shown to be highly specific for myocardial damage and to have sensitivity comparable with that of creatine kinase MB isoenzyme for detecting cardiac injury. Furthermore, increases of cTnI persist in plasma for at least several days. The present study was designed to determine the relative sensitivities of cTnI and LD isoenzymes over time for the diagnosis of infarction. The results indicate that cTnI values are at least as sensitive as LD isoenzymes: 90% of patients with myocardial infarction had above-normal concentrations of cTnI on the 4th day after admission to the coronary care unit. Criteria based on cTnI should improve the accuracy of retrospective diagnoses of acute myocardial infarction.

Oxytocin exerts protective effects on in vitro myocardial injury induced by ischemia and reperfusionThis article is one of a selection of papers from the NATO Advanced Research Workshop on Translational Knowledge for Heart Health (published in part 1 of a 2-part Special Issue).

2009 ◽  
Vol 87 (2) ◽  
pp. 137-142 ◽  
Author(s):  
Maria Ondrejcakova ◽  
Tatiana Ravingerova ◽  
Jan Bakos ◽  
Dezider Pancza ◽  
Daniela Jezova
Keyword(s):  
Infarct Size ◽  
Myocardial Injury ◽  
Ischemia Reperfusion ◽  
Cardiac Injury ◽  
Myocardial Damage ◽  
Control Group ◽  
Protective Effects ◽  
Chronotropic Effect ◽  
Negative Chronotropic Effect

Among the cardiovascular pathologies, ischemic heart disease is a serious medical problem that can result in cardiac injury and (or) heart failure. The aim of the present study was to test the hypothesis that neuropeptide oxytocin induces cardioprotective effects on ischemia–reperfusion-induced myocardial damage. The functional parameters of isolated Langendorff-perfused rat hearts were recorded before and after global 25 min ischemia and subsequent reperfusion. The infarct size was determined by a computerized planimetric method. The results showed that oxytocin produced negative chronotropic effect even at low concentrations (90–125 nmol/L). Perfusion with oxytocin before ischemia resulted in significant reduction of the infarct size (p < 0.01), which was about 66% smaller than that in the control group. To evaluate the functional mechanisms involved, further experiments were performed under conditions of constant heart rate. The lower dose of oxytocin (90 nmol/L), which was ineffective in spontaneously beating hearts, induced a significant decrease of contractility. Elimination of the negative chronotropic effect of oxytocin prevented its cardioprotective action. In conclusion, our results demonstrated an attenuation of the infarct size in oxytocin-treated hearts, indicating a cardioprotective effect of oxytocin. The data suggest that the negative chronotropic action of oxytocin participates in its protective effects on ischemia–reperfusion-induced myocardial injury.

scholarly journals Liposomal Resveratrol and/or Carvedilol Attenuate Doxorubicin-Induced Cardiotoxicity by Modulating Inflammation, Oxidative Stress and S100A1 in Rats

Antioxidants ◽  
2020 ◽  
Vol 9 (2) ◽  
pp. 159
Author(s):  
Abeer M. Alanazi ◽  
Laila Fadda ◽  
Ahlam Alhusaini ◽  
Rehab Ahmad ◽  
Iman H. Hasan ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cell Injury ◽  
Troponin I ◽  
Chemotherapeutic Agents ◽  
Protective Effects ◽  
Potent Effect ◽  
Histological Alterations ◽  
Endoplasmic Reticulum Calcium ◽  
Creatine Kinase Mb ◽  
Oxide Synthase

Doxorubicin (DOX) is a cytotoxic anthracycline antibiotic and one of the important chemotherapeutic agents for different types of cancers. DOX treatment is associated with adverse effects, particularly cardiac dysfunction. This study examined the cardioprotective effects of carvedilol (CAR) and/or resveratrol (RES) and liposomal RES (LIPO-RES) against DOX-induced cardiomyopathy, pointing to their modulatory effect on oxidative stress, inflammation, S100A1 and sarco/endoplasmic reticulum calcium ATPase2a (SERCA2a). Rats received CAR (30 mg/kg) and/or RES (20 mg/kg) or LIPO-RES (20 mg/kg) for 6 weeks and were challenged with DOX (2 mg/kg) twice per week from week 2 to week 6. DOX-administered rats exhibited a significant increase in serum creatine kinase-MB (CK-MB), troponin-I and lactate dehydrogenase (LDH) along with histological alterations, reflecting cardiac cell injury. Cardiac toll-like receptor 4 (TLR-4), inducible nitric oxide synthase (iNOS), tumor necrosis factor (TNF)-α and interleukin (IL)-6 protein expression were up-regulated, and lipid peroxidation was increased in DOX-administered rats. Treatment with CAR, RES or LIPO-RES as well as their alternative combinations ameliorated all observed biochemical and histological alterations with the most potent effect exerted by CAR/LIPO-RES. All treatments increased cardiac antioxidants, and the expression of S100A1 and SERCA2a. In conclusion, the present study conferred new evidence on the protective effects of CAR and its combination with either RES or LIPO-RES on DOX-induced inflammation, oxidative stress and calcium dysregulation.

scholarly journals Propofol Through Upregulating Caveolin-3 Attenuates Post-Hypoxic Mitochondrial Damage and Cell Death in H9C2 Cardiomyocytes During Hyperglycemia

2017 ◽  
Vol 44 (1) ◽  
pp. 279-292 ◽  
Author(s):  
Fan Deng ◽  
Shuang Wang ◽  
Liangqing Zhang ◽  
Xiang Xie ◽  
Shuyun Cai ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Mitochondrial Dysfunction ◽  
Cell Injury ◽  
Troponin I ◽  
Ischemia Reperfusion ◽  
Antioxidant Properties ◽  
Underlying Mechanism ◽  
Mitochondrial Damage ◽  
Protective Effects ◽  
Creatine Kinase Mb

Background/Aims: Hearts from diabetic subjects are susceptible to myocardial ischemia reperfusion (I/R) injury. Propofol has been shown to protect against myocardial I/R injury due to its antioxidant properties while the underlying mechanism remained incompletely understood. Thus, this study aimed to determine whether or not propofol could attenuate myocardial I/R injury by attenuating mitochondrial dysfunction/damage through upregulating Caveolin (Cav)-3 under hyperglycemia. Methods: Cultured rat cardiomyocyte H9C2 cells were subjected to hypoxia/reoxygenation (H/R) in the absence or presence of propofol under high glucose (HG), and cell viability, lactate dehydrogenase (LDH) and mitochondrial viability as well as creatine kinase-MB (CK-MB), cardiac troponin I (cTnI) and intracellular adenosine triphosphate (ATP) content were measured with colorimetric Enzyme-Linked Immunosorbent Assays. Intracellular levels of oxidative stress was assessed using 2,7-dichlorodihydrofluorescein diacetate (DCF-DA) fluorescent staining and mitochondrial-dependent apoptosis was assessed by detecting mitochondrial membrane potential and the activation of apoptotic caspases 3 and 9. Results: Exposure of cells to HG without or with H/R both significantly increased cell injury, cell apoptosis and enhanced oxidative stress that were associated with mitochondrial dysfunction and decreased Cav-3 protein expression. All these changes were further exacerbated following H/R under HG. Administration of propofol at concentrations from 12.5 to 50 µM but not 100 µM significantly attenuated H/R injury that was associated with increased Cav-3 expression and activation of the prosurvival proteins Akt and STAT3 with the optimal protective effects seen at 50 µM of propofol (P25). The beneficial effects of propofol(P25) were abrogated by Cav-3 disruption with β-methyl-cyclodextrin. Conclusion: Propofol counteracts cardiomyocyte H/R injury by attenuating mitochondrial damage and improving mitochondrial biogenesis through upregulating Cav-3 during hyperglycemia.

Abstract 060: CCN1/a 6 β 1 Mediates Myocardial Injuries Induced by Work Overload or by Doxorubicin in Mice

2013 ◽  
Vol 113 (suppl_1) ◽  
Author(s):  
Pei-Ling I Hsu ◽  
Fan-E Mo
Keyword(s):  
Myocardial Injury ◽  
Fas Ligand ◽  
Cardiac Injury ◽  
Pressure Overload ◽  
Myocardial Damage ◽  
Matricellular Protein ◽  
Work Overload ◽  
Myocardial Injuries ◽  
Injury Models

Introduction: Matricellular protein CCN1 is expressed in myocardial infarction, pressure overload, and ischemia in mice, and in patients with a failing heart. Despite its well-documented angiogenic activities, CCN1 promotes fibroblast apoptosis in some contexts. The role of CCN1 in an injured heart was not clear. We assessed the hypothesis that CCN1 plays a detrimental role and mediates cardiac injury through its proapoptotic activities. Methods and Results: To test the role of CCN1 in cardiac injury, we employed two different myocardial injury models in mice, including a work-overload-induced injury created by isoproterenol treatment (ISO; 100 mg/kg/day; s.c. for 5 days; n= 6 for each group) and an injury induced by the cardiotoxicity of doxorubicin (DOX, single dose of 15 mg/kg; i.p. sacrificed after 14 days). Ccn1 expression was induced in the damaged myocardium in both injury models. A line of knock-in mice carrying an apoptosis-defective Ccn1 mutant allele, Ccn1-dm , which has disrupted integrin α 6 β 1 binding sites, were tested in the ISO- or DOX -induced cardiac injury. Myocardial damage was seen in tissues from wile-type (WT) hearts after receiving ISO. Ccn1 dm/dm (DM) mice possessed remarkable resistance against ISO or DOX treatments and exhibited no tissue damage or fibrosis compared to WT mice after H&E or Masson’s trichrome stainings. DM mice were resistant to both ISO- and DOX-induced cardiac cell apoptosis, indicating that CCN1 is critically mediating cardiomyocyte apoptotic death in cardiac injury. Moreover, we found that death factor Fas ligand (FasL) and its receptor Fas were upregulated in WT mice receiving ISO or DOX treatments by immunohistochemical staining, compared with the PBS-control. 8-OHdG-positive, a marker for oxidative stress, cardiomyocytes were increased by ISO or DOX treatments as well. In contrast, the expression of Fas/FasL, and the 8-OHdG-positive cardiomyocytes in the myocardium of DM mice were not changed by ISO or DOX. Conclusions: We identify CCN1 as a novel pathophysiological regulator of cardiomyocyte apoptosis in cardiac injury. Blocking apoptotic function of CCN1 effectively prevents myocardial injury in mice. CCN1 and its receptor α 6 β 1 represent promising future therapeutic targets in cardiac injury.

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.

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