scholarly journals Cardioprotective Effects of Tualang Honey: Amelioration of Cholesterol and Cardiac Enzymes Levels

2015 ◽  
Vol 2015 ◽  
pp. 1-8 ◽  
Author(s):  
Md. Ibrahim Khalil ◽  
E. M. Tanvir ◽  
Rizwana Afroz ◽  
Siti Amrah Sulaiman ◽  
Siew Hua Gan
Keyword(s):  
Lipid Peroxidation ◽  
Troponin I ◽  
Histopathological Examination ◽  
Antioxidant Defense System ◽  
Protective Effects ◽  
Marker Enzymes ◽  
Cardiac Marker ◽  
Creatine Kinase Mb ◽  
Cardioprotective Effects ◽  
Tualang Honey

The present study was designed to investigate the cardioprotective effects of Malaysian Tualang honey against isoproterenol- (ISO-) induced myocardial infarction (MI) in rats by investigating changes in the levels of cardiac marker enzymes, cardiac troponin I (cTnI), triglycerides (TG), total cholesterol (TC), lipid peroxidation (LPO) products, and antioxidant defense system combined with histopathological examination. Male albino Wistar rats (n= 40) were pretreated orally with Tualang honey (3 g/kg/day) for 45 days. Subcutaneous injection of ISO (85 mg/kg in saline) for two consecutive days caused a significant increase in serum cardiac marker enzymes (creatine kinase-MB (CK-MB), lactate dehydrogenase (LDH), and aspartate transaminase (AST)), cTnI, serum TC, and TG levels. In addition, ISO-induced myocardial injury was confirmed by a significant increase in heart lipid peroxidation (LPO) products (TBARS) and a significant decrease in antioxidant enzymes (SOD, GPx, GRx, and GST). Pretreatment of ischemic rats with Tualang honey conferred significant protective effects on all of the investigated biochemical parameters. The biochemical findings were further confirmed by histopathological examination in both Tualang-honey-pretreated and ISO-treated hearts. The present study demonstrates that Tualang honey confers cardioprotective effects on ISO-induced oxidative stress by contributing to endogenous antioxidant enzyme activity via inhibition of lipid peroxidation.

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 Cardioprotective Potential of Polyphenolic Rich Green Combination in Catecholamine Induced Myocardial Necrosis in Rabbits

2015 ◽  
Vol 2015 ◽  
pp. 1-9 ◽  
Author(s):  
Fatiqa Zafar ◽  
Nazish Jahan ◽  
Khalil-Ur-Rahman ◽  
Ahrar Khan ◽  
Waseem Akram
Keyword(s):  
Oxidative Stress ◽  
Antioxidant Enzymes ◽  
Histopathological Examination ◽  
Cardiac Injury ◽  
Myocardial Necrosis ◽  
Myocardial Cell ◽  
Marker Enzymes ◽  
Cardiac Marker ◽  
Synthetic Drugs ◽  
Plant Mixture

The present study was designed to develop safer, effective, and viable cardioprotective herbal combination to control oxidative stress related cardiac ailments as new alternatives to synthetic drugs. The synergetic cardioprotective potential of herbal combination of four plantsT. arjuna(T.A.),P. nigrum(P.N),C. grandiflorus(C), andC. oxyacantha(Cr) was assessed through curative and preventive mode of treatment. In preventive mode of treatment, the cardiac injury was induced with synthetic catecholamine (salbutamol) to pretreated rabbits with the proposed herbal combination for three weeks. In curative mode of treatment, cardiotoxicity/oxidative stress was induced in rabbits with salbutamol prior to treating them with plant mixture. Cardiac marker enzymes, lipids profile, and antioxidant enzymes as biomarker of cardiotoxicity were determined in experimental animals. Rabbits administrated with mere salbutamol showed a significant increase in cardiac marker enzymes and lipid profile and decrease in antioxidant enzymes as compared to normal control indicating cardiotoxicity and myocardial cell necrosis. However, pre- and postadministration of plant mixture appreciably restored the levels of all biomarkers. Histopathological examination confirmed that the said combination was safer cardioprotective product.

scholarly journals Supplementation of Lipoic Acid, Zinc and Clopidogrel Reduces Mortality Rate and Incidence of Ventricular Arrhythmia in Experimental Myocardial Infarction

2021 ◽  
Vol 12 ◽  
Author(s):  
Enas Abdel-Hady ◽  
Fatma Mohamed ◽  
Mona Ahmed ◽  
Mohamed Abdel-Salam ◽  
Mahmoud Ayobe
Keyword(s):  
Myocardial Infarction ◽  
Mortality Rate ◽  
Lipoic Acid ◽  
Plasma Levels ◽  
Troponin I ◽  
Heart Diseases ◽  
Hypolipidemic Effect ◽  
Protective Effects ◽  
Adrenergic Stimulation ◽  
Creatine Kinase Mb

Despite the significant advances in management of coronary heart diseases, myocardial infarction (MI) is still associated with a high mortality rate. The present study was planned to investigate the possible protective effects of the anti-oxidants lipoic acid and zinc sulfate as well as the anti-platelet clopidogrel on cardiac dysfunction in experimental isoproterenol (ISO)-induced MI, aiming at achieving useful means for protection and therapy against MI. Wistar rats of both sexes were allocated into five groups: control, untreated MI and MI pre-treated with lipoic acid, zinc, or clopidogrel. All rats were subjected to ECG recording and measurement of plasma levels of troponin I, creatine kinase-MB (CK-MB) unit, triglycerides and total cholesterol. The hearts were isolated and studied on Langendorff preparation for assessment of intrinsic cardiac activities. The results revealed that the percent mortality was markedly reduced upon pre-treatment and the total arrhythmia was also decreased except for the zinc pre-treated rats. The ST-segment elevation was significantly reduced and the plasma levels of CK-MB were only decreased in lipoic acid and clopidogrel pre-treated rats with variable hypolipidemic effect. Hearts of clopidogrel pre-treated rats showed augmented inotropic activity both basal and in response to β-adrenergic stimulation. While zinc pre-treated hearts revealed improved rate of contraction and increased myocardial flow rate. Overall, these results indicate that lipoic acid, zinc and clopidogrel were variably effective in modifying the ISO-induced MI insults and offered partial protection against experimental myocardial damage.

scholarly journals Cardioprotective potential of polyphenols rich Thraatchathi Chooranam against isoproterenol induced myocardial necrosis in experimental rats

2020 ◽  
Vol 20 (1) ◽  
Author(s):  
Ramakrishnan Ganapathy ◽  
Anita Ramachandran ◽  
Sushmitha Basavapattana Shivalingaiah ◽  
Muhammed Bishir ◽  
Saravanan Bhojaraj ◽  
...  
Keyword(s):  
Troponin I ◽  
Histopathological Examination ◽  
Antioxidant Properties ◽  
Membrane Integrity ◽  
Myocardial Necrosis ◽  
Experimental Period ◽  
High Dose ◽  
Dependent Manner ◽  
Protective Effects ◽  
Cardiac Tissues

Abstract Background The present study establishes the cardioprotective role of Thraatchathi Chooranam (TC), a polyherbal traditional Siddha medicine, in terms of membrane stabilizing and antioxidant properties in isoproterenol (ISO) induced myocardial necrosis model in rats. Methods Animals were divided into six groups (n = 6), normal (received vehicle 0.5% CMC, p.o.), ISO control (received 0.5% CMC + ISO 120 mg/kg, b.w. s.c. twice at an interval of 48 h), standard control (received Vit-E 100 mg/kg, p.o.) + ISO, TC low and high dose (50 and 100 mg/kg p.o., respectively) + ISO, and drug control (received TC at 100 mg/kg, p.o.). At the end of experimental period, blood samples collected and plasma cardiac troponin-I (CTn-I) was measured by ELISA. Cardiac tissues were isolated, levels of membrane stabilizing enzymes, antioxidants and inflammatory markers were estimated. Gene expression of Bax, Bcl2, Caspase 3, HIF-α, TNF-α, iNOS, TRX1 and TrxR were performed by RT-PCR. Histopathological studies on cardiac tissues were conducted using hematoxylin and eosin (H&E) stain. Statistical analyses were performed by one-way ANOVA followed by Tukey’s multiple comparison as post-hoc test. Results Administration of ISO resulted in a significant increase in plasma CTn-I, decrease in superoxide dismutase, glutathione and glutathione peroxidase; it also significantly altered membrane stabilizing enzymes like Na+/K+-ATPase, Mg2+-ATPase Ca2+-ATPase and Cathepsin D. Pretreatment with TC (50 mg/kg and 100 mg/kg) decreased CTn-I, and improved membrane stabilizing and endogenous antioxidant enzymes and decreased cathespin D level in a dose dependent manner. Histopathological examination revealed that TC improves cellular membrane integrity and decreases inflammatory cell infiltration and necrotic death. Conclusion The present study provided a strong evidence on the protective effects of TC against ISO-induced myocardial necrosis in rats.

Protective effects of olmesartan and l-carnitine on doxorubicin-induced cardiotoxicity in rats

2020 ◽  
Vol 98 (4) ◽  
pp. 183-193 ◽  
Author(s):  
Malek M. Aziz ◽  
Mai A. Abd El Fattah ◽  
Kawkab A. Ahmed ◽  
Helmy M. Sayed
Keyword(s):  
Transforming Growth Factor Beta ◽  
Troponin I ◽  
Transforming Growth Factor ◽  
Antineoplastic Agent ◽  
The Other ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Group I ◽  
Creatine Kinase Mb

Doxorubicin (DOX), an anthracycline antibiotic, is an important antineoplastic agent due to its high antitumor efficacy in hematological as well as in solid malignancies. The clinical use of DOX is limited due to its cardiotoxic effects. The present study aimed to investigate the possible protective effect of olmesartan (Olm), l-carnitine (L-CA), and their combination in cardiotoxicity induced by DOX in rats. Male albino rats were randomly divided into seven experimental groups (n = 8): group I: normal control, group II: L-CA, group III: Olm, group IV: DOX. The other three groups were treated with Olm (10 mg/kg), L-CA (300 mg/kg), and their combination for 2 weeks after induction of cardiotoxicity by a single dose of DOX (20 mg/kg). In the results, DOX showed a significant elevation in serum troponin I, creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH) together with increased inflammation manifested by the rise of tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecules-1 (ICAM-1), interleukin IL-1β (IL-1β), myeloperoxidase (MPO), nuclear factor-kappa B (NF-κB), and transforming growth factor beta (TGF-β) in cardiac tissues as well as DOX-induced oxidative stress by increasing in malondialdehyde (MDA) and decreasing in superoxide dismutase (SOD) and glutathione (GSH) in heart tissues. In addition, caspase-3 activity was boosted as indication of increased apoptosis. On the other hand, administration of L-CA and Olm attenuated the DOX-evoked disturbances in the abovementioned parameters. In addition, DOX exhibited echocardiographic changes and severe histopathological changes, which were significantly reversed by L-CA and Olm treatment. In conclusion, the present study data confirm the protective role of L-CA and Olm in DOX-induced cardiotoxicity, which may be related to its antioxidant, antiinflammatory, and antiapoptotic agents.

scholarly journals Tualang Honey Protects against BPA-Induced Morphological Abnormalities and Disruption of ERα, ERβ, and C3 mRNA and Protein Expressions in the Uterus of Rats

2015 ◽  
Vol 2015 ◽  
pp. 1-18 ◽  
Author(s):  
Siti Sarah Mohamad Zaid ◽  
Normadiah M. Kassim ◽  
Shatrah Othman
Keyword(s):  
Lipid Peroxidation ◽  
Protective Effects ◽  
Oral Gavage ◽  
Concurrent Treatment ◽  
Endocrine Disrupting Chemical ◽  
Morphological Abnormalities ◽  
Normal Functions ◽  
Endocrine Disrupting ◽  
Protein Expressions ◽  
Tualang Honey

Bisphenol A (BPA) is an endocrine disrupting chemical (EDC) that can disrupt the normal functions of the reproductive system. The objective of the study is to investigate the potential protective effects of Tualang honey against BPA-induced uterine toxicity in pubertal rats. The rats were administered with BPA by oral gavage over a period of six weeks. Uterine toxicity in BPA-exposed rats was determined by the degree of the morphological abnormalities, increased lipid peroxidation, and dysregulated expression and distribution of ERα, ERβ, and C3 as compared to the control rats. Concurrent treatment of rats with BPA and Tualang honey significantly improved the uterine morphological abnormalities, reduced lipid peroxidation, and normalized ERα, ERβ, and C3 expressions and distribution. There were no abnormal changes observed in rats treated with Tualang honey alone, comparable with the control rats. In conclusion, Tualang honey has potential roles in protecting the uterus from BPA-induced toxicity, possibly accounted for by its phytochemical properties.

Hydrogen sulfide ameliorates cardiovascular dysfunction induced by cecal ligation and puncture in rats

2015 ◽  
Vol 34 (10) ◽  
pp. 953-964 ◽  
Author(s):  
RS Abdelrahman ◽  
MS El-Awady ◽  
MA Nader ◽  
EM Ammar
Keyword(s):  
Hydrogen Sulfide ◽  
Vascular Reactivity ◽  
Troponin I ◽  
Histopathological Examination ◽  
Vascular Dysfunction ◽  
Cecal Ligation ◽  
Cecal Ligation And Puncture ◽  
Cardiovascular Dysfunction ◽  
Sodium Hydrosulfide ◽  
Creatine Kinase Mb

Hydrogen sulfide (H2S) is an endogenously produced gaseous messenger that participates in regulation of cardiovascular functions. This study evaluates the possible protective effect of H2S in cardiovascular dysfunction induced by cecal ligation and puncture (CLP) in rats. After 24 h of induction of CLP, heart rate (HR), mortality, cardiac and inflammation biomarkers (creatine kinase-MB (CK-MB) isozyme, cardiac troponin I (cTnI), C-reactive protein (CRP), and lactate dehydrogenase (LDH)), in vitro vascular reactivity, histopathological examination, and oxidative biomarkers (malondialdehyde (MDA), reduced glutathione (GSH), and superoxide dismutase (SOD)) were determined. CLP induced elevations in HR, mortality, serum CK-MB, cTnI, CRP, and LDH, in addition to impaired aortic contraction to potassium chloride and phenylephrine and relaxation to acetylcholine without affecting sodium nitroprusside responses. Moreover, CLP increased cardiac and aortic MDA and decreased SOD, without affecting GSH and caused a marked subserosal and interstitial inflammation in endocardium. Sodium hydrosulfide, but not the irreversible inhibitor of H2S synthesis dl-propargyl glycine, protected against CLP-induced changes in HR, mortality, cardiac and inflammatory biomarkers, oxidative stress, and myocardium histopathological changes without affecting vascular dysfunction. Our results confirm that H2S can attenuate CLP-induced cardiac, but not vascular, dysfunction possibly through its anti-inflammatory and antioxidant effects.

scholarly journals Protective Effect of Silymarin against Acrolein-Induced Cardiotoxicity in Mice

2012 ◽  
Vol 2012 ◽  
pp. 1-14 ◽  
Author(s):  
Elahe Taghiabadi ◽  
Mohsen Imenshahidi ◽  
Khalil Abnous ◽  
Fatemeh Mosafa ◽  
Mojtaba Sankian ◽  
...  
Keyword(s):  
Protective Effect ◽  
Caspase 3 ◽  
Troponin I ◽  
Environmental Pollutants ◽  
Protective Effects ◽  
Histopathological Changes ◽  
Cardiac Tissues ◽  
Creatine Kinase Mb ◽  
Serum Cardiac Troponin ◽  
Cytosolic Cytochrome

Reactiveα,β-unsaturated aldehydes such as acrolein (ACR) are major components of environmental pollutants and have been implicated in the neurodegenerative and cardiac diseases. In this study, the protective effect of silymarin (SN) against cardiotoxicity induced by ACR in mice was evaluated. Studies were performed on seven groups of six animals each, including vehicle-control (normal saline + 0.5% w/v methylcellulose), ACR (7.5 mg/kg/day, gavage) for 3 weeks, SN (25, 50 and 100 mg/kg/day, i.p.) plus ACR, vitamin E (Vit E, 100 IU/kg, i.p.) plus ACR, and SN (100 mg/kg, i.p.) groups. Mice received SN 7 days before ACR and daily thereafter throughout the study. Pretreatment with SN attenuated ACR-induced increased levels of malondialdehyde (MDA), serum cardiac troponin I (cTnI), and creatine kinase-MB (CK-MB), as well as histopathological changes in cardiac tissues. Moreover, SN improved glutathione (GSH) content, superoxide dismutase (SOD), and catalase (CAT) activities in heart of ACR-treated mice. Western blot analysis showed that SN pretreatment inhibited apoptosis provoked by ACR through decreasing Bax/Bcl-2 ratio, cytosolic cytochrome c content, and cleaved caspase-3 level in heart. In conclusion, SN may have protective effects against cardiotoxicity of ACR by reducing lipid peroxidation, renewing the activities of antioxidant enzymes, and preventing apoptosis.

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