Seabuckthorn Attenuates Cardiac Dysfunction and Oxidative Stress in Isoproterenol-Induced Cardiotoxicity in Rats

2011 ◽  
Vol 30 (6) ◽  
pp. 671-680 ◽  
Author(s):  
Salma Malik ◽  
Sameer Goyal ◽  
Shreesh Kumar Ojha ◽  
Saurabh Bharti ◽  
Saroj Nepali ◽  
...  
Keyword(s):  
Cardiac Dysfunction ◽  
Antioxidant Activities ◽  
Cardiac Injury ◽  
Radical Scavenging ◽  
Myocardial Necrosis ◽  
Myocardial Damage ◽  
Ultrastructural Changes ◽  
And Oxidative Stress ◽  
Preventive Role

We investigated the effects of seabuckthorn (SBT) oil in isoproterenol (ISO)-induced cardiotoxicity with reference to hemodynamic, antioxidant, histopathological, and ultrastructural parameters. Rats were administered SBT oil (5, 10, and 20 mL/kg per d) or vehicle orally for 30 days along with ISO (85 mg/kg, subcutaneously, at 24-hour interval) on 29th and 30th day. On 31st day, ISO control rats showed cardiac dysfunction, increased lipid peroxidation, depletion of cardiac injury marker enzymes, and antioxidant activities. Myocardial necrosis, edema, and inflammation were evident from the light microscopic and ultrastructural changes. Seabuckthorn oil at the dose of 20 mL/kg per d significantly modulates hemodynamic and antioxidant derangements. The preventive role of SBT oil on ISO-induced cardiotoxicity was reconfirmed by histopathological and ultrastructural examinations. Thus, the present study reveals that SBT oil mitigates myocardial damage in ISO-induced cardiac injury in rats by maintaining hemodynamic, biochemical, histopathological, and ultrastructural perturbations owing to its free radical scavenging and antioxidant activities.

Study of antioxidant potential in leaves, stems, nuts of Juglans regia L.

2012 ◽  
Vol 1 (10) ◽  
pp. 79 ◽  
Author(s):  
G. Raja* ◽  
Ivvala Anand Shaker ◽  
Inampudi Sailaja ◽  
R. Swaminathan ◽  
S. Saleem Basha ◽  
...  
Keyword(s):  
Free Radicals ◽  
Free Radical ◽  
Antioxidant Activities ◽  
Radical Scavenging Activity ◽  
Juglans Regia ◽  
Radical Scavenging ◽  
Antioxidant Compounds ◽  
Free Radical Damage ◽  
Radical Damage

Natural antioxidants can protect the human body from free radicals and retard the progress of many chronic diseases as well as lipid oxidative rancidity in foods. The role of antioxidants has protected effect against free radical damage that may cause many diseases including cancer. Primary sources of naturally occurring antioxidants are known as whole grains, fruits, and vegetables. Several studies suggest that regular consumption of nuts, mostly walnuts, may have beneficial effects against oxidative stress mediated diseases such as cardiovascular disease and cancer. The role of antioxidants has attracted much interest with respect to their protective effect against free radical damage that may cause many diseases including cancer. Juglans regia L. (walnut) contains antioxidant compounds, which are thought to contribute to their biological properties. Polyphenols, flavonoids and flavonols concentrations and antioxidant activity of Leaves, Stems and Nuts extract of Juglans regia L. as evaluated using DPPH, ABTS, Nitric acid, hydroxyl and superoxide radical scavenging activity, lipid peroxidation and total oxidation activity were determined. The antioxidant activities of Leaves, Stems and Nuts extract of Juglans regia L. were concentration dependent in different experimental models and it was observed that free radicals were scavenged by the test compounds in all the models.

scholarly journals Molecular Mechanisms of Obesity-Linked Cardiac Dysfunction: An Up-Date on Current Knowledge

Cells ◽  
2021 ◽  
Vol 10 (3) ◽  
pp. 629
Author(s):  
Jorge Gutiérrez-Cuevas ◽  
Ana Sandoval-Rodriguez ◽  
Alejandra Meza-Rios ◽  
Hugo Christian Monroy-Ramírez ◽  
Marina Galicia-Moreno ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cardiac Dysfunction ◽  
Molecular Mechanisms ◽  
Current Knowledge ◽  
Peroxisome Proliferator ◽  
White Adipocyte ◽  
Peroxisome Proliferator Activated Receptors ◽  
And Oxidative Stress

Obesity is defined as excessive body fat accumulation, and worldwide obesity has nearly tripled since 1975. Excess of free fatty acids (FFAs) and triglycerides in obese individuals promote ectopic lipid accumulation in the liver, skeletal muscle tissue, and heart, among others, inducing insulin resistance, hypertension, metabolic syndrome, type 2 diabetes (T2D), atherosclerosis, and cardiovascular disease (CVD). These diseases are promoted by visceral white adipocyte tissue (WAT) dysfunction through an increase in pro-inflammatory adipokines, oxidative stress, activation of the renin-angiotensin-aldosterone system (RAAS), and adverse changes in the gut microbiome. In the heart, obesity and T2D induce changes in substrate utilization, tissue metabolism, oxidative stress, and inflammation, leading to myocardial fibrosis and ultimately cardiac dysfunction. Peroxisome proliferator-activated receptors (PPARs) are involved in the regulation of carbohydrate and lipid metabolism, also improve insulin sensitivity, triglyceride levels, inflammation, and oxidative stress. The purpose of this review is to provide an update on the molecular mechanisms involved in obesity-linked CVD pathophysiology, considering pro-inflammatory cytokines, adipokines, and hormones, as well as the role of oxidative stress, inflammation, and PPARs. In addition, cell lines and animal models, biomarkers, gut microbiota dysbiosis, epigenetic modifications, and current therapeutic treatments in CVD associated with obesity are outlined in this paper.

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.

Role of intracellular antioxidant enzymes after in vivo myocardial ischemia and reperfusion

2003 ◽  
Vol 284 (1) ◽  
pp. H277-H282 ◽  
Author(s):  
Steven P. Jones ◽  
Michaela R. Hoffmeyer ◽  
Brent R. Sharp ◽  
Ye-Shih Ho ◽  
David J. Lefer
Keyword(s):  
Antioxidant Enzymes ◽  
Glutathione Peroxidase ◽  
Ischemia Reperfusion ◽  
Myocardial Necrosis ◽  
Myocardial Damage ◽  
Ischemia And Reperfusion ◽  
Myocardial Ischemia And Reperfusion

Reactive oxygen species induce myocardial damage after ischemia and reperfusion in experimental animal models. Numerous studies have investigated the deleterious effects of ischemia-reperfusion (I/R)-induced oxidant production using various pharmacological interventions. More recently, in vitro studies have incorporated gene-targeted mice to decipher the role of antioxidant enzymes in myocardial reperfusion injury. We examined the role of cellular antioxidant enzymes in the pathogenesis of myocardial I/R (MI/R) injury in vivo in gene-targeted mice. Neither deficiency nor overexpression of Cu-Zn superoxide dismutase (SOD) altered the extent of myocardial necrosis. Overexpression of glutathione peroxidase did not affect the degree of myocardial injury. Conversely, overexpression of manganese (Mn)SOD significantly attenuated myocardial necrosis after MI/R. Transthoracic echocardiography was performed on MnSOD-overexpressing and wild-type mice that were subjected to a more prolonged period of reperfusion. Cardiac output was significantly depressed in the nontransgenic but not the transgenic MnSOD-treated mice. Anterior wall motion was significantly impaired in the nontransgenic mice. These findings demonstrate an important role for MnSOD but not Cu/ZnSOD or glutathione peroxidase in mice after in vivo MI/R.

scholarly journals The Role of C-8 OH on the Antioxidant Activity of Norwogonin and Isowogonin

2020 ◽  
Vol 15 (5) ◽  
pp. 1934578X2092488
Author(s):  
Qiushan Zhang ◽  
Jin Shao ◽  
Tong Zhao ◽  
Lei He ◽  
Huiping Ma ◽  
...  
Keyword(s):  
Antioxidant Activity ◽  
Ferrous Iron ◽  
Antioxidant Activities ◽  
Radical Scavenging ◽  
Iron Chelation ◽  
Reducing Power ◽  
Antioxidant Property ◽  
Hydroxyl Group ◽  
Total Antioxidant

In the present study, the antioxidant property of 4 flavones (moslosooflavone, wogonin, isowogonin, and norwogonin) was evaluated using 6 different assays: 1,1-diphenyl-2-picrylhydrazyl (DPPH·), superoxide (O2 •−), and nitric oxide (NO) radical scavenging assays, ferrous iron chelation, reducing power, and total antioxidant capacity. The 4 flavones exhibited antioxidant activities with decreasing order as norwogonin > isowogonin >> wogonin> moslosooflavone. The present results demonstrated that norwogonin and isowogonin exhibited excellent antioxidant activity, which was mainly based on the presence of C-8 hydroxyl group.

scholarly journals ROLE OF THE GENETIC FACTORS, DETOXICATION SYSTEMS AND OXIDATIVE STRESS IN THE PATHOGENESIS OF ENDOMETRIOSIS AND INFERTILITY (REVIEW)

2013 ◽  
Vol 68 (8) ◽  
pp. 14-19 ◽  
Author(s):  
E. D. Dubinskaya ◽  
A. S. Gasparov ◽  
T. A. Fedorova ◽  
N. V. Lapteva
Keyword(s):  
Oxidative Stress ◽  
Genetic Factors ◽  
Antioxidant Activities ◽  
Polycystic Ovary ◽  
Reproductive Function ◽  
Detoxification Enzyme ◽  
Systemic Oxidative Stress ◽  
Exogenous Factors ◽  
And Oxidative Stress

The aim of this paper is to provide a systematic review of the role of the genetic factors, detoxication systems and oxidative stress in the pathogenesis of endometriosis and infertility. Endometriosis and infertility are still both the most uncommon diseases in gynecology. Many aspects of female reproductive function are strongly influenced by genetic factors, and numerous studies have attempted to identify susceptibility genes for disorders affecting female fertility such as polycystic ovary syndrome, endometriosis, fibroids, cancer (ovarian, vulvar, cervical), premature ovarian failure, recurrent pregnancy loss and pre-eclampsia. The most solid evidence linking specific polymorphisms to endometriosis is showed by the studies investigating a phase II detoxification enzyme. No data were found concerning influences of the genetic factors on the female infertility. Contrary, a lot of studies devoted to the genetic factors of male infertility are presented. It’s known that endometriosis associated with increased systemic oxidative stress. The implication of increased systemic oxidative stress in disease progression or the association with other oxidative stress-related pathologic conditions needs to be addressed in further studies. The majority of studies suggest a reduced antioxidant capacity in infertile women with endometriosis. In the present review we discussed the role of the genetic factors in the pathogenesis of endometriosis and infertility. NAT2 polimorphism, xenobiotic methabolism and exogenous factors are somehow related with these diseases. An altered balance between pro-oxidant and antioxidant activities may have an impact on folliculogenesis and adequate embryo development. 

scholarly journals Autophagy inhibition enables Nrf2 to exaggerate the progression of diabetic cardiomyopathy in mice

2020 ◽  
Author(s):  
Ada Admin ◽  
Huimei Zang ◽  
Weiwei Wu ◽  
Lei Qi ◽  
Wenbin Tan ◽  
...  
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Cardiac Dysfunction ◽  
Antioxidant Defense ◽  
Myocardial Damage ◽  
Related Factor ◽  
Nrf2 Knockout ◽  
Underlying Mechanisms ◽  
Autophagy Inhibition ◽  
And Oxidative Stress

Nuclear factor-erythroid factor 2-related factor 2 (Nrf2) may either ameliorate or worsen diabetic cardiomyopathy. However, the underlying mechanisms are poorly understood. Herein we report a novel mechanism of Nrf2-mediated myocardial damage in type 1 diabetes (T1D). Global Nrf2 knockout (Nrf2KO) hardly affected the onset of cardiac dysfunction induced by T1D but slowed down its progression in mice independent of sex. In addition, Nrf2KO inhibited cardiac pathological remodeling, apoptosis and oxidative stress associated with both onset and advancement of cardiac dysfunction in T1D. Such Nrf2-mediated progression of diabetic cardiomyopathy was confirmed by cardiomyocyte-restricted (CR) Nrf2 transgenic (Tg) approach in mice. Moreover, cardiac autophagy inhibition via CR KO of autophagy related 5 gene (CR-Atg5KO) led to early onset and accelerated development of cardiomyopathy in T1D, and CR-Atg5KO-induced adverse phenotypes were rescued by additional Nrf2KO. Mechanistically, chronic T1D leads to glucolipotoxicity inhibiting autolysosome efflux, which in turn intensifies Nrf2-driven transcription to fuel lipid peroxidation while inactivating Nrf2-mediated antioxidant defense and impairing Nrf2-coordinated iron metabolism, thereby leading to ferroptosis in cardiomyocytes. These results demonstrate that diabetes over time causes autophagy deficiency, which turns off Nrf2-mediated defense while switching on Nrf2-operated pathological program toward ferroptosis in cardiomyocytes, thereby worsening the progression of diabetic cardiomyopathy.

scholarly journals Role of Carvedilol in Prevention of Adrenaline Induced Myocardial Infraction in Experimental Animal

2016 ◽  
Vol 12 (2) ◽  
pp. 127-134
Author(s):  
Wahida Rahman ◽  
Nargis Akhter ◽  
Md Abrar Hossain ◽  
Sayeda Nazrina
Keyword(s):  
Free Radical ◽  
Reduced Glutathione ◽  
Myocardial Necrosis ◽  
Myocardial Damage ◽  
Antioxidant Property ◽  
Free Radical Production ◽  
Group Iii ◽  
Radical Production ◽  
Group I

Introduction: Acute myocardial infarction (AMI) is the most important form of ischemic heart disease (IHD). Coronary artery disease (CAD) is an increasingly important medical and public health problem and is the leading cause of mortality in Bangladesh. AMI is the rapid development of myocardial necrosis caused by a critical imbalance between the oxygen supply and demand of the myocardium. Total occlusion of the coronary arteries for more than 4-6 hrs results in irreversible myocardial necrosis, but reperfusion within this period can salvage the myocardium and reduce morbidity and mortality. Objectives: To assess the role of carvedilol in prevention of adrenaline induced cardiac damage in experimental animal. Materials and Methods: This experimental study was carried out in the department of pharmacology, Bangabandhu Sheikh Mujib Medical University (BSMMU), Dhaka for a period of One year spanning from July 2004 to June 2005. Fifty two healthy rats of Long Evan Norwegian strains, 3-4 months of ages of both sexes, weight between 180-220g were used. The experiment was divided into two parts: Part-I and Part-II. Thirty two rats were selected for Part-I experiment and subdivided into Group-I and Group-II. In Part-II experiment, 20 rats were selected and placed as Group-III. Group-I (12 rats) of control group was treated with 02 doses of inj distilled water (D/W) subcutaneously (S.C.) 24 hrs apart and serum creatine kinase-MB (CK-MB) level and hepatic and cardiac reduced glutathione (GSH) contents were estimated from 06 (Group-Ia) rats after 12 hrs and serum aspartate aminotransferase (AST) level and hepatic and cardiac reduced GSH contents were estimated from 06 (Group-Ib) rats after 24 hrs of 2nd inj of D/W. Group-II (20 rats) was treated with 02 doses of inj adrenaline (2mg/kg) S.C. in 24 hrs interval and in above mentioned way serum CK-MB level, GSH (hepatic and cardiac) contents and serum AST and GSH (hepatic and cardiac) contents were estimated 12 hrs and 24 hrs after the 2nd inj of adrenaline respectively. In experimental group (Group-III) all the rats (20) were treated with carvedilol (1 mg/kg) orally for 14 consecutive days and then were given 02 doses of inj adrenaline with the interval of 24 hrs and again serum CK-MB level and GSH (hepatic and cardiac) contents were estimated from half of the rats (10) after 12 hrs of injection and serum AST level and GSH (hepatic and cardiac) contents were measured from half of the rats (10) after 24 hrs of 2nd injection of adrenaline. Results: Adrenaline (2mg/kg) induced myocardial damage was evaluated biochemically by significant (P˂0.001) increase in CK-MB and AST levels. Free radical production following adrenaline induced myocardial damage was reflected by significant (P˂0.001) depletion in hepatic and cardiac reduced glutathione (GSH) contents. Cardioprotection provided by carvedilol pretreatment in adrenaline induced myocardial infarction was assessed by significant prevention of increase in serum CK-MB and AST levels. Antioxidant property of carvedilol was evaluated by significant (P<0.001) prevention of depletion in hepatic and cardiac GSH contents. The results of the study indicated that carvedilol pretreatment provided effective prevention in adrenaline induced myocardial damage and also provided effective antioxidative action. Conclusion: This study indicated that adrenaline administration induced myocardial damage as evidenced by increase in serum CK-MB and AST levels which was associated with free radical production as reflected by depletion in hepatic and cardiac GSH contents. It was observed that carvedilol through their antioxidant property in addition to their β-blocking effect prevents free radical mediated injury of catecholamine assault following MI. Journal of Armed Forces Medical College Bangladesh Vol.12(2) 2016: 127-134

scholarly journals Parvovirus Infection Is Associated With Myocarditis and Myocardial Fibrosis in Young Dogs

2017 ◽  
Vol 54 (6) ◽  
pp. 964-971 ◽  
Author(s):  
Jordan Ford ◽  
Laura McEndaffer ◽  
Randall Renshaw ◽  
Alex Molesan ◽  
Kathleen Kelly
Keyword(s):  
In Situ Hybridization ◽  
Myocardial Fibrosis ◽  
Messenger Rna ◽  
Cardiac Injury ◽  
Myocardial Necrosis ◽  
Myocardial Damage ◽  
Conventional Polymerase Chain Reaction ◽  
Cardiac Damage ◽  
Myocardial Lesions

Perinatal parvoviral infection causes necrotizing myocarditis in puppies, which results in acute high mortality or progressive cardiac injury. While widespread vaccination has dramatically curtailed the epidemic of canine parvoviral myocarditis, we hypothesized that canine parvovirus 2 (CPV-2) myocardial infection is an underrecognized cause of myocarditis, cardiac damage, and/or repair by fibrosis in young dogs. In this retrospective study, DNA was extracted from formalin-fixed, paraffin-embedded tissues from 40 cases and 41 control dogs under 2 years of age from 2007 to 2015. Cases had a diagnosis of myocardial necrosis, inflammation, or fibrosis, while age-matched controls lacked myocardial lesions. Conventional polymerase chain reaction (PCR) and sequencing targeting the VP1 to VP2 region detected CPV-2 in 12 of 40 cases (30%; 95% confidence interval [CI], 18%–45%) and 2 of 41 controls (5%; 95% CI, 0.1%–16%). Detection of CPV-2 DNA in the myocardium was significantly associated with myocardial lesions ( P = .003). Reverse transcription quantitative PCR amplifying VP2 identified viral messenger RNA in 12 of 12 PCR-positive cases and 2 of 2 controls. PCR results were confirmed by in situ hybridization, which identified parvoviral DNA in cardiomyocytes and occasionally macrophages of juvenile and young adult dogs (median age 61 days). Myocardial CPV-2 was identified in juveniles with minimal myocarditis and CPV-2 enteritis, which may indicate a longer window of cardiac susceptibility to myocarditis than previously reported. CPV-2 was also detected in dogs with severe myocardial fibrosis with in situ hybridization signal localized to cardiomyocytes, suggesting prior myocardial damage by CPV-2. Despite the frequency of vaccination, these findings suggest that CPV-2 remains an important cause of myocardial damage in dogs.

scholarly journals Autophagy inhibition enables Nrf2 to exaggerate the progression of diabetic cardiomyopathy in mice

2020 ◽  
Author(s):  
Ada Admin ◽  
Huimei Zang ◽  
Weiwei Wu ◽  
Lei Qi ◽  
Wenbin Tan ◽  
...  
Keyword(s):  
Diabetic Cardiomyopathy ◽  
Cardiac Dysfunction ◽  
Antioxidant Defense ◽  
Myocardial Damage ◽  
Related Factor ◽  
Nrf2 Knockout ◽  
Underlying Mechanisms ◽  
Autophagy Inhibition ◽  
And Oxidative Stress

Nuclear factor-erythroid factor 2-related factor 2 (Nrf2) may either ameliorate or worsen diabetic cardiomyopathy. However, the underlying mechanisms are poorly understood. Herein we report a novel mechanism of Nrf2-mediated myocardial damage in type 1 diabetes (T1D). Global Nrf2 knockout (Nrf2KO) hardly affected the onset of cardiac dysfunction induced by T1D but slowed down its progression in mice independent of sex. In addition, Nrf2KO inhibited cardiac pathological remodeling, apoptosis and oxidative stress associated with both onset and advancement of cardiac dysfunction in T1D. Such Nrf2-mediated progression of diabetic cardiomyopathy was confirmed by cardiomyocyte-restricted (CR) Nrf2 transgenic (Tg) approach in mice. Moreover, cardiac autophagy inhibition via CR KO of autophagy related 5 gene (CR-Atg5KO) led to early onset and accelerated development of cardiomyopathy in T1D, and CR-Atg5KO-induced adverse phenotypes were rescued by additional Nrf2KO. Mechanistically, chronic T1D leads to glucolipotoxicity inhibiting autolysosome efflux, which in turn intensifies Nrf2-driven transcription to fuel lipid peroxidation while inactivating Nrf2-mediated antioxidant defense and impairing Nrf2-coordinated iron metabolism, thereby leading to ferroptosis in cardiomyocytes. These results demonstrate that diabetes over time causes autophagy deficiency, which turns off Nrf2-mediated defense while switching on Nrf2-operated pathological program toward ferroptosis in cardiomyocytes, thereby worsening the progression of diabetic cardiomyopathy.

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