Pentoxifylline Attenuates Arsenic Trioxide-Induced Cardiac Oxidative Damage in Mice

This study was undertaken to evaluate the therapeutic potential effect of pentoxifylline (PTX) against arsenic trioxide (ATO)-induced cardiac oxidative damage in mice. Thirty-six male albino mice were divided into six groups and treated intraperitoneally with normal saline (group 1), ATO (5 mg/kg; group 2), PTX (100 mg/kg; group 3), and different doses of PTX (25, 50, and 100 mg/kg; groups 4, 5, and 6, respectively) with ATO. After four weeks, the blood sample was collected for biochemical experiments. In addition, cardiac tissue was removed for assessment of oxidative stress markers and histopathological changes (such as hemorrhage, necrosis, infiltration of inflammatory cells, and myocardial degeneration). The findings showed that ATO caused a significant raise in serum biochemical markers such as lactate dehydrogenase (LDH), creatine phosphokinase (CPK) and troponin-I (cTnI), glucose, total cholesterol (TC), and triglyceride (TG) levels. In addition to histopathological changes in cardiac tissue, ATO led to the significant increase in cardiac lipid peroxidation (LPO) and nitric oxide (NO); remarkable decrease in the activity of cardiac antioxidant enzymes such as catalase (CAT), superoxide dismutase (SOD), and glutathione peroxidase (GPx); and the depletion of the total antioxidant capacity (TAC) and total thiol groups (TTGs). PTX was able to reduce the increased levels of serum cardiac markers (LDH, CPK, cTnI, TC, and TG), cardiac LPO, and improve antioxidant markers (TAC, TTGs, CAT, SOD, and GPx) alongside histopathologic changes. However, no significant changes were observed in elevated serum glucose and cardiac NO levels. In conclusion, the current study showed the potential therapeutic effect of PTX in the prevention of ATO-induced cardiotoxicity via reversing the oxidative stress.

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Abstract 305: Nebivolol Confers Mitochondria-Targeted Cardioprotection in Isoproterenol-Induced Acute Stressor State

Circulation Research ◽

10.1161/res.111.suppl_1.a305 ◽

2012 ◽

Vol 111 (suppl_1) ◽

Author(s):

Sumeet S Vaikunth ◽

Karl T Weber ◽

Syamal K Bhattacharya

Keyword(s):

Oxidative Stress ◽

Cardiac Tissue ◽

Mitochondrial Permeability Transition ◽

Therapeutic Potential ◽

Permeability Transition Pore ◽

Permeability Transition ◽

Antioxidant Defenses ◽

Sprague Dawley ◽

Acute Stressor ◽

And Oxidative Stress

Introduction: Isoproterenol-induced acute stressor state simulates injury from burns or trauma, and results in Ca 2+ overloading and oxidative stress in diverse tissues, including cardiac myocytes and their subsarcolemmal mitochondria (SSM), overwhelming endogenous Zn 2+ -based antioxidant defenses. We hypothesized that pretreatment with nebivolol (Nebi), having dual beta-1 antagonistic and novel beta-3 receptor agonistic properties, would prevent Ca 2+ overloading and oxidative stress and upregulate Zn 2+ -based antioxidant defenses, thus enhancing its overall cardioprotective potential in acute stressor state. Methods: Eight-week-old male Sprague-Dawley rats received a single subcutaneous dose of isoproterenol (1 mg/kg) and compared to those treated with Nebi (10 mg/kg by gavage) for 10 days prior to isoproterenol. SSM were harvested from cardiac tissue at sacrifice. Total Ca 2+ , Zn 2+ and 8-isoprostane levels in tissue, and mitochondrial permeability transition pore (mPTP) opening, free [Ca 2+ ] m and H 2 O 2 production in SSM were monitored. Untreated, age-/sex-matched rats served as controls; each group had six rats and data shown as mean±SEM. Results: Compared to controls, isoproterenol rats revealed: (1) Significantly (*p<0.05) increased cardiac tissue Ca 2+ (8.2±0.8 vs. 13.7±1.0*, nEq/mg fat-free dry tissue (FFDT)), which was abrogated ( # p<0.05) by Nebi (8.9±0.4 # ); (2) Reduced cardiac Zn 2+ (82.8±2.4 vs. 78.5±1.0*, ng/mg FFDT), but restored by Nebi (82.4±0.6 # ); (3) Two-fold rise in cardiac 8-isoprostane (111.4±13.7 vs. 232.1±17.2*, pmoles/mg protein), and negated by Nebi (122.3+14.5 # ); (4) Greater opening propensity for mPTP that diminished by Nebi; (5) Elevated [Ca 2+ ] m (88.8±2.5 vs. 161.5±1.0*, nM), but normalized by Nebi (93.3±2.7 # ); and (6) Increased H 2 O 2 production by SSM (97.4±5.3 vs. 142.8±7.0*, pmoles/mg protein/min), and nullified by Nebi (106.8±9.0 # ). Conclusions : Cardioprotection conferred by Nebi, a unique beta-blocker, prevented Ca 2+ overloading and oxidative stress in cardiac tissue and SSM, while simultaneously augmenting antioxidant capacity and promoting mPTP stability. Therapeutic potential of Nebi in patients with acute stressor states remains a provocative possibility that deserves to be explored.

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Clerodendrum volubile Ethanol Leaf Extract: A Potential Antidote to Doxorubicin-Induced Cardiotoxicity in Rats

Journal of Toxicology ◽

10.1155/2020/8859716 ◽

2020 ◽

Vol 2020 ◽

pp. 1-17 ◽

Cited By ~ 1

Author(s):

Olufunke Esan Olorundare ◽

Adejuwon Adewale Adeneye ◽

Akinyele Olubiyi Akinsola ◽

Daniel Ayodele Sanni ◽

Mamoru Koketsu ◽

...

Keyword(s):

Oxidative Stress ◽

Cardiac Tissue ◽

Troponin I ◽

Histopathological Examination ◽

Radical Scavenging ◽

Oxidative Stress Marker ◽

Oxidative Stress Markers ◽

Dry Extract ◽

Stress Markers ◽

Antioxidant Mechanisms

Doxorubicin is widely applied in hematological and solid tumor treatment but limited by its off-target cardiotoxicity. Thus, cardioprotective potential and mechanism(s) of CVE in DOX-induced cardiotoxicity were investigated using cardiac and oxidative stress markers and histopathological endpoints. 50–400 mg/kg/day CVE in 5% DMSO in distilled water were investigated in Wistar rats intraperitoneally injected with 2.5 mg/kg DOX on alternate days for 14 days, using serum troponin I and LDH, complete lipid profile, cardiac tissue oxidative stress marker assays, and histopathological examination of DOX-treated cardiac tissue. Preliminary qualitative and quantitative assays of CVE’s secondary metabolites were also conducted. Phytochemical analyses revealed the presence of flavonoids (34.79 ± 0.37 mg/100 mg dry extract), alkaloids (36.73 ± 0.27 mg/100 mg dry extract), reducing sugars (07.78 ± 0.09 mg/100 mg dry extract), and cardiac glycosides (24.55 ± 0.12 mg/100 mg dry extract). 50–400 mg/kg/day CVE significantly attenuated increases in the serum LDH and troponin I levels. Similarly, the CVE dose unrelatedly decreased serum TG and VLDL-c levels without significant alterations in the serum TC, HDL-c, and LDL-c levels. Also, CVE profoundly attenuated alterations in the cardiac tissue oxidative stress markers’ activities while improving DOX-associated cardiac histological lesions that were possibly mediated via free radical scavenging and/or antioxidant mechanisms. Overall, CVE may play a significant therapeutic role in the management of DOX-induced cardiotoxicity in humans.

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3, 4-Dihydroxyphenylethanol attenuates cadmium-induced oxidative stress, inflammation and apoptosis in rat heart

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v18i4.5 ◽

2021 ◽

Vol 18 (4) ◽

pp. 713-719

Author(s):

Yan Huang ◽

Hongsheng Gang ◽

Bitao Liang ◽

Ming Li

Keyword(s):

Oxidative Stress ◽

Cardiac Tissue ◽

Troponin I ◽

Heart Tissue ◽

Cardiac Markers ◽

Tnf Α ◽

Protein Expressions ◽

Tissue Homogenates ◽

Induced Apoptosis ◽

Pro Inflammatory Cytokines

Purpose: To investigate the therapeutic effect of 3, 4-dihydroxyphenylethanol (DOPET) on cadmium (Cd) induced cardiotoxicity in murine model. Methods: Four groups of rats were used in this study (n = 6). The rats were treated with DOPET and Cd for 28 days. Biochemical parameters were determined in plasma and heart tissue homogenates. Results: Cadmium (Cd) significantly increased lipid peroxidation and protein carbonylation. However, DOPET treatment significantly attenuated Cd-induced oxidative stress. Cd intoxication significantly increased cardiac markers {creatine kinase, lactate dehydrogenase (LDH) and cardiac troponin-I} levels in plasma, and reduced the levels of antioxidants such as superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase Gpx ,glutathione (GSH) and malndialdehyde (MDA) in heart tissue. These Cdinduced changes in cardiac markers and antioxidants were reversed by DOPET treatment. Cd treatment led to upregulation of protein expressions of pro-inflammatory cytokines (TNF-α and Il-6). However, DOPET supplementation brought about a decrease in the protein expressions of these cytokines. Western blot analysis revealed that Cd induced apoptosis in cardiac tissue, as was evident from alterations in protein expressions of the apoptotic inducers, Bax and cleaved caspase-3, and the anti-apoptotic factor Bcl-2. However, DOPET treatment effectively reversed Cd-induced apoptosis. Conclusion: These results indicate that DOPET exerts cardio-protective effect against Cd-induced toxicity via antioxidant, anti-inflammatory and anti-apoptotic mechanisms.

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Nano-Curcumin Prevents Cardiac Injury, Oxidative Stress and Inflammation, and Modulates TLR4/NF-κB and MAPK Signaling in Copper Sulfate-Intoxicated Rats

Antioxidants ◽

10.3390/antiox10091414 ◽

2021 ◽

Vol 10 (9) ◽

pp. 1414

Author(s):

Wedad S. Sarawi ◽

Ahlam M. Alhusaini ◽

Laila M. Fadda ◽

Hatun A. Alomar ◽

Awatif B. Albaker ◽

...

Keyword(s):

Oxidative Stress ◽

Copper Sulfate ◽

Troponin I ◽

Tissue Injury ◽

Cardiac Injury ◽

Elevated Serum ◽

Mapk Signaling ◽

Mitogen Activated Protein Kinase ◽

Native Form ◽

Tnf Α

Copper (Cu) is essential for a plethora of biological processes; however, its high redox reactivity renders it potentially toxic. This study investigated the protective effect of curcumin (CUR) and nano-CUR (N-CUR) against Cu cardiotoxicity, emphasizing the role of oxidative stress, TLR4/NF-κB and mitogen-activated protein kinase (MAPK) signaling and cell death in rats. Rats received 100 mg/kg copper sulfate (CuSO4), a pesticide used for repelling pests, and were concurrently treated with CUR or N-CUR for 7 days. Cu caused cardiac injury manifested by elevated serum cardiac troponin I (cTnI), creatine kinase (CK)-MB, and lactate dehydrogenase (LDH), as well as histopathological alterations. Cardiac malondialdehyde (MDA), NF-κB p65, TNF-α, and IL-6 were increased, and reduced glutathione (GSH), superoxide dismutase (SOD) and catalase were decreased in Cu-treated rats. CUR and N-CUR prevented cardiac tissue injury, decreased serum cTnI, CK-MB, and LDH, and cardiac MDA, NF-κB p65, TNF-α, and IL-6, and enhanced cellular antioxidants. CUR and N-CUR downregulated TLR4 and AP-1, and decreased the phosphorylation levels of p38 MAPK, JNK, and ERK1/2. In addition, CUR and N-CUR increased cardiac Bcl-2 and BAG-1, decreased Bax and caspase-3, and prevented DNA fragmentation. In conclusion, N-CUR prevents Cu cardiotoxicity by attenuating oxidative injury, inflammatory response, and apoptosis, and modulating TLR4/NF-κB and MAPK signaling. The cardioprotective effect of N-CUR was more potent than the native form.

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Therapeutic Effect of Bilsaan, Sambucus nigra Stem Exudate, on the OVA-Induced Allergic Asthma in Mice

Oxidative Medicine and Cellular Longevity ◽

10.1155/2020/3620192 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Faris Alrumaihi ◽

Ahmad Almatroudi ◽

Khaled S. Allemailem ◽

Arshad H. Rahmani ◽

Arif Khan ◽

...

Keyword(s):

Oxidative Stress ◽

Immune Responses ◽

Allergic Asthma ◽

Therapeutic Effect ◽

Therapeutic Potential ◽

Inflammatory Cells ◽

Lavage Fluid ◽

Alveolar Wall ◽

Sambucus Nigra ◽

The Status

Asthma is characterized by the elevated level of Th2 immune responses, oxidative stress, and airway inflammation. Bilsaan, an exudate from the stem of Sambucus nigra, has been traditionally used in the treatment of various ailments in Saudi Arabia. Here, we investigated the therapeutic potential of Bilsaan against ovalbumin- (OVA-) induced allergic asthma in a mouse model. In order to induce allergic asthma, mice were intraperitoneally injected with alum-emulsified-OVA (20 μg/mouse) on days 0, 14, and 21 that is followed by an intranasal OVA exposure from days 22 to 30. During this time, mice were orally administered with Bilsaan at the doses of 5, 10, and 25 mg/kg. The numbers of total and differential inflammatory cells and the levels of Th2 cytokines (IL-4, IL-5, and IL-13) and IgE were determined in bronchoalveolar lavage fluid (BALF). Moreover, the therapeutic effect of Bilsaan was also assessed to analyze the oxidative stress and inflammatory changes in the lung tissues. The results demonstrated that Bilsaan treatment significantly reduced the total and differential inflammatory cell count in the BALF. The BALF from the mice treated with Bilsaan showed significantly lower levels of IL-4, IL-5, IL-13, and IgE. Interestingly, a similar pattern was observed in IL-4, IL-5, and IL-13 secreted by OVA-sensitized splenocytes from the mice of various groups. Bilsaan treatment alleviated the status of oxidative stress by modulating malondialdehyde (MDA), superoxide dismutase (SOD), and catalase levels in the lung. Moreover, Bilsaan treatment reduced the infiltration of inflammatory cells, thickening of alveolar wall, and congestion in the lung tissues. The findings of the present study demonstrated an antiasthmatic effect of Bilsaan through the modulation of Th2 immune responses, inflammation, and the oxidative stress.

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Suppression of lncRNA LINC00472 Prevents Amyloid-β-induced Neurotoxicity in PC12 Cells via Regulating miR-141-3p/Foxo3 Axis

10.21203/rs.3.rs-331635/v1 ◽

2021 ◽

Author(s):

Min Guo ◽

Jilai Li ◽

Peifu Wang ◽

Di Jin

Keyword(s):

Oxidative Stress ◽

Oxidative Damage ◽

Neuronal Death ◽

Matched Control ◽

Therapeutic Potential ◽

Amyloid Β ◽

Luciferase Reporter ◽

Synaptic Connections ◽

Key Features ◽

Pro Inflammatory Cytokines

Abstract Alzheimer's Disease (AD) is characterized by the accumulations of amyloid-β (Aβ) plaques and neurofibrillary tangles in brain, dysfunctions and loss of synaptic connections, exaggerated inflammation, and eventually neuronal death. Oxidative damage may explain the key features and suggest the therapeutic potential to prevent AD progression, yet it remains largely elusive the occurrence and thus the interventions of oxidative damage. Besides, miRNA dysregulation is tightly associated with AD progression. By recruiting 30 AD patients and 30 age-matched control, we demonstrated the upregulations of LINC00472, pro-inflammatory cytokines and ROS in the serum of AD subjects. Similar results were reproduced in Aβ treated SH-SY5Y cells. In addition, through luciferase reporter and RNA pull-down assays, we revealed direct interactions between LINC00472 and miR-141-3p, and between miR-141-3p and FOXO3 and the signalling loop LINC00472/miR-141-3p/FOXO3 loop is involved in Aβ administration induced oxidative stress. Moreover, we raised evidence that knocking down LINC00472 in SH-SY5Y cells ameliorated the Aβ administration induced oxidative stress. Thus, normalization of LINC00472 may be therapeutic to retard AD progression via ameliorating oxidative stress. Future works may further strengthen the pharmacological potentials of interventions for AD progression by targeting LINC00472/ miR-141-3p/ FOXO3 loop.

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Coenzyme Q10 attenuates airway inflammation and oxidative stress in neonatal asthmatic rats

Tropical Journal of Pharmaceutical Research ◽

10.4314/tjpr.v19i9.24 ◽

2020 ◽

Vol 19 (9) ◽

pp. 1969-1975

Author(s):

Jingwei Peng ◽

Jilong Ma ◽

Lan Zhang ◽

Banghao Lu

Keyword(s):

Oxidative Stress ◽

Lipid Peroxidation ◽

Airway Inflammation ◽

Coenzyme Q10 ◽

Therapeutic Potential ◽

Inflammatory Cells ◽

Th2 Cytokines ◽

Gene Expressions ◽

Keywords Asthma ◽

And Oxidative Stress

Purpose: To determine the therapeutic effect of coenzyme Q10 (CoQ10) on ovalbumin (OVA)-provoked asthma in neonatal rats.Methods: Asthma was induced by exposing neonatal rats to OVA. The levels of SOD, CAT, GPx, GSH, MDA and MPO were estimated using standard biochemical kits, while ELISA was used to measure the concentrations of Ig E and Th2 cytokines. Gene expressions were assayed with qRT-PCR, and protein expressions were determined with western blotting.Results: OVA treatment led to increases in levels of BALF inflammatory cells, lipid peroxidation, serum IgE and BALF Th2 cytokines, but it decreased antioxidant levels. Furthermore, the protein expression of NF-κB and mRNA expression levels of proinflammatory cytokines and inducible nitric oxide synthase (iNOS) were upregulated in the asthmatic rats (p < 0.05). However, coenzyme Q10 supplementation significantly decreased lipid peroxidation, and reduced inflammatory cells and IgE levels, while the antioxidant levels were enhanced (p < 0.05). Moreover, coenzyme Q10 reduced the levels of Th2 cytokines and downregulated the expressions of NF-κB, TNF-α, IL-6, and iNOS in the neonatal asthmatic rats (p < 0.05).Conclusion: Coenzyme Q10 attenuates airway inflammation and oxidative stress in neonatal asthmatic rats. Thus, coenzyme Q10 has promising therapeutic potential in the management of asthma. Keywords: Asthma, Neonatal, Coenzyme Q10, Th2, cytokines, Oxidative stress, Antiinflammation

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Protective Effects of Quercetin on Livers from Mice Exposed to Long-Term Cigarette Smoke

BioMed Research International ◽

10.1155/2020/2196207 ◽

2020 ◽

Vol 2020 ◽

pp. 1-10

Author(s):

Pedro A. Machado-Junior ◽

Natália P. S. Araújo ◽

Ana B. F. Souza ◽

Thalles F. Castro ◽

Michel Oliveira ◽

...

Keyword(s):

Oxidative Stress ◽

Inflammatory Response ◽

Cigarette Smoke ◽

Liver Diseases ◽

Inflammatory Cells ◽

Smoke Exposure ◽

Cigarette Smoke Exposure ◽

Protective Effects ◽

Histopathological Changes

Cigarette smoke is highly toxic, and it can promote increased production of reactive species and inflammatory response and leads to liver diseases. Quercetin is a flavonoid that displays antioxidant and anti-inflammatory activities in liver diseases. This study aimed at evaluating the protective effects of quercetin on livers from mice exposed to long-term cigarette smoke exposure. Male C57BL/6 mice were divided into five groups: control (CG), vehicle (VG), quercetin (QG), cigarette smoke (CSG), quercetin, and cigarette smoke (QCSG). CSG and QCSG were exposed to cigarette smoke for sixty consecutive days; at the end of the exposures, all animals were euthanized. Mice that received quercetin daily and were exposed to cigarette smoke showed a reduced influx of inflammatory cells, oxidative stress, inflammatory reaction, and histopathological changes in the liver, compared to CSG. These results suggest that quercetin may be an effective adjuvant for treating damage to the liver due to cigarette smoke exposure.

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7-Chloro-4-(phenylselanyl) quinoline reduces renal oxidative stress induced by oxaliplatin in mice

Canadian Journal of Physiology and Pharmacology ◽

10.1139/cjpp-2021-0090 ◽

2021 ◽

Author(s):

Ketlyn P. da Motta ◽

Briana B. Lemos ◽

Jaini J. Paltian ◽

Angélica S Reis ◽

Gustavo B. Blödorn ◽

...

Keyword(s):

Oxidative Stress ◽

Superoxide Dismutase ◽

Oxidative Damage ◽

Aminolevulinic Acid ◽

Therapeutic Potential ◽

Thiobarbituric Acid ◽

Protein Carbonyl ◽

Glutathione S Transferase ◽

Protein Thiol ◽

The Relationship

Purpose: evaluating the relationship between oxidative damage oxaliplatin (OXA)-induced and the therapeutic potential of 7-chloro-4-(phenylselanyl) quinoline (4-PSQ) in kidney of mice. Methods: Mice received OXA (10 mg/kg) or vehicle by intraperitoneal route (days 0 and 2). Oral administration of 4-PSQ (1 mg/kg) or vehicle was performed on days 2 to 14. On day 15, the animals were euthanized, and the kidneys and blood collected. The effect of OXA and/or 4-PSQ on urea, thiobarbituric acid reactive species (TBARS), non-protein thiol (NPSH) and protein carbonyl (PC) levels were investigated. Moreover, renal superoxide dismutase (SOD), catalase (CAT), glutathione peroxidase (GPx), glutathione reductase (GR), glutathione S-transferase (GST), δ-aminolevulinic acid dehydratase (δ-ALA-D) and Na+, K+ ATPase activities were evaluated. Results: Our findings revealed an increase on urea levels and a significant renal oxidative damage in OXA-induced mice. OXA exposure increased SOD, GPx and GST activities and caused a reduction on NPSH levels, CAT and GR activities. Na+, K+ ATPase and -ALA-D activities were reduced by OXA. 4-PSQ decreased plasmatic urea levels and renal oxidative damage. SOD, GPx, CAT, GR and Na+, K+ ATPase activities were restored by 4-PSQ. Conclusion: 4-PSQ may be a good prototype for the treatment of OXA-induced renal injury.

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Evaluating the protective potency of Acacia hydaspica R. Parker on histological and biochemical changes induced by Cisplatin in the cardiac tissue of rats

BMC Complementary and Alternative Medicine ◽

10.1186/s12906-019-2575-8 ◽

2019 ◽

Vol 19 (1) ◽

Cited By ~ 5

Author(s):

Tayyaba Afsar ◽

Suhail Razak ◽

Ali Almajwal ◽

Maria Shabbir ◽

Muhammad Rashid Khan

Keyword(s):

Oxidative Stress ◽

Creatine Kinase ◽

Antioxidant Enzymes ◽

Cardiac Function ◽

Cardiac Tissue ◽

Troponin I ◽

Antioxidant Properties ◽

Oxidative Stress Markers ◽

Oxidative Stress Biomarkers ◽

Stress Markers

Abstract Background Increase oxidative trauma is the main cause behind Cisplatin (CP) induced cardiotoxicity which restricts its clinical application as anti-neoplastic prescription. Acacia hydaspica is a natural shrub with diverse bioactivities. Acacia hydaspica ethyl acetate extract (AHE) ameliorated drug-induced cardiotoxicity in animals with anti-oxidative mechanisms. Current study aimed to evaluate the protective potential of A. hydaspica against cisplatin-induced myocardial injury. Methods Rats were indiscriminately distributed into six groups (n = 6). Group 1: control; Groups 2: Injected with CP (7.5 mg/kg bw, i.p, single dose) on day 16; Group 3: Treated for 21 days with AHE (400 mg/kg b.w, oral); Group 4: Received CP injection on day 16 and treated with AHE for 5 days post injection; Group 5: Received AHE (400 mg/kg b.w/day, p.o.) for 21 days and CP (7.5 mg/kg b.w., i.p.) on day 16; Group 6: Treated with silymarin (100 mg/kg b.w., p.o.) after 1 day interval for 21 days and CP injection (7.5 mg/kg b.w., i.p.) on day 16. On 22nd day, the animals were sacrificed and their heart tissues were removed. Cisplatin induced cardiac toxicity and the influence of AHE were evaluated by examination of serum cardiac function markers, cardiac tissue antioxidant enzymes, oxidative stress markers and histology. Results CP inoculation considerably altered cardiac function biomarkers in serum and diminished the antioxidant enzymes levels, while increased oxidative stress biomarkers in cardiac tissues AHE treatment attenuated CP-induced deteriorations in creatine kinase (CK), Creatine kinase isoenzymes MB (CK-MB), cardiac Troponin I (cTNI) and lactate dehydrogenase (LDH) levels and ameliorated cardiac oxidative stress markers as evidenced by decreasing lipid peroxidation, H2O2 and NO content along with augmentation in phase I and phase II antioxidant enzymes. Additionally, CP inoculation also induced morphological alterations which were ameliorated by AHE. In pretreatment group more significant protection was observed compared to post-treatment group indicating preventive potential of AHE. The protective potency of AHE was comparable to silymarin. Conclusion Results demonstrate that AHE attenuated CP induce cardiotoxicity. The polyphenolic metabolites and antioxidant properties of AHE might be responsible for its protective influence.

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