Allicin ameliorates doxorubicin-induced cardiotoxicity in rats via suppression of oxidative stress, inflammation and apoptosis

Abdel-Daim, Mohamed M.; Kilany, Omnia; Khalifa, Hesham A.; Ahmed, Amira

doi:10.1007/s00280-017-3413-7

Cited by 132 publications

(83 citation statements)

References 52 publications

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“…The treatments were carried out for a period of 30 days. The dose duration of TMX treatment was previously shown to be toxic but not lethal . The doses of FWEP (100 mg/kg and 200 mg/kg of diet) were shown in previous studies to be effective in lowering toxicity …”

Section: Methodsmentioning

confidence: 98%

“…Recently, more attention has been paid to the protective effects of natural antioxidants against chemical‐induced cardiomyocytes injury . Herbal medicines and their bioactive compounds such as lycopene, mirazid ( Commiphora molmol ) and ascorbic acid, allicin, parsley oil, phytochemicals from Aerva lanata, Aronia melanocarpa, Astragalus polysaccharide, Bombyx mori, Astragalus polysaccharide, Azadirachta indica, Bombyx mori, and Allium stavium and Spirulina have been used to reduce free radical‐production and to treat cardiotoxicity induced by pesticides, chemicals and drugs.…”

Section: Introductionmentioning

confidence: 99%

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Cardiotoxicity and myocardial infarction‐associated DNA damage induced by thiamethoxam in vitro and in vivo: Protective role of Trigonella foenum‐graecum seed‐derived polysaccharide

Feki

Saad

Bkhairia

et al. 2018

Environmental Toxicology

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The risk of pesticides on the human health and environment has drawn increasing attention. Today, new tools are developed to reduce pesticide adverse effects. This study aimed to evaluate the toxicity induced by, thiamethoxam (TMX), and the cytoprotective effect of a novel polysaccharide, named fenugreek seed water polysaccharide (FWEP) in vitro using H9c2 cardiomyoblastes and in vivo using Wistar rat model. Animals were assigned into four groups per eight rats each: group 1 served as a control group, group 2 received TMX, group 3, and group 4 received both FWEP and TMX tested at two doses (100 and 200 mg/kg, respectively). Regarding the in vitro study, our results demonstrated that TMX induced a decrease in H9c2 cell viability up to 70% with the highest concentration. In vivo, TMX injection induced marked heart damage noted by a significant increase in plasma lactate dehydrogenase, creatine phosphokinase, troponin-T, aspartate amino transferase activities, cholesterol, and triglyceride levels. Concomitant alterations in cardiac antioxidant defense system revealed depletion in the levels of glutathione and non-protein thiol and an increase in the activity of superoxide dismutase, catalase, and glutathione peroxidase. Similarly, a significant increase in heart lipid, malondialdehyde, advanced oxidation protein product and in protein carbonyls levels was also noted. In addition, heart tissues histo-architecture displayed major presence of apoptosis and necrosis as confirmed by DNA degradation. However, supplementation with FWEP alleviated heart oxidative damage and genotoxicity. In this manner, ABTS radical-scavenging activity, linoleic acid oxidation tests and heart genomic and DNA nicking assay had proved FWEP strong antioxidant potential. In conclusion, FWEP provided significant protection against TMX-induced heart injury, and could be a useful and efficient agent against cardiotoxicity and atherosclerosis. K E Y W O R D S cardiotoxicity, cytotoxicity, oxidative stress, polysaccharide, thiamethoxam

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Section: Methodsmentioning

confidence: 98%

Section: Introductionmentioning

confidence: 99%

Cardiotoxicity and myocardial infarction‐associated DNA damage induced by thiamethoxam in vitro and in vivo: Protective role of Trigonella foenum‐graecum seed‐derived polysaccharide

Feki

Saad

Bkhairia

et al. 2018

Environmental Toxicology

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“…However, some mechanisms, such as oxidative stress, excessive calcium, and cytokine release were recorded. Among these possible mechanisms, the oxidative stress hypothesis is still the cornerstone [Bruynzeel et al, 2007;Saeed et al, 2015;El-Agamy et al, 2016;Abdel-Daim et al, 2017;Shahidullah et al, 2017]. Induction of free radicals and other toxic nonradicals released from cells by anthracyclines can be neutralized by generating endogenous antioxidants or by introducing exogenous antioxidants in nutritional supplements [Abushouk et al, 2017].…”

Section: Introductionmentioning

confidence: 99%

Ameliorative Effect of Cardamom Aqueous Extract on Doxorubicin-Induced Cardiotoxicity in Rats

Gazia¹,

El-Magd²

2018

Cells Tissues Organs

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This study was conducted to evaluate the potential cardioprotective effect of cardamom (CAR) against myocardial injuries induced by doxorubicin (DOX) in rats through investigation of histological alterations and the associated oxidative stress, apoptosis, inflammation, and angiogenesis. This study included 30 adult male albino rats that were randomized to 3 groups (n = 10/group): group I (control), group II (DOX) rats injected with DOX (2.5 mg/kg body weight [BW] i.p.) every other day for 2 weeks, and group III (CAR+DOX) received CAR extract (200 mg/kg BW) orally for 3 weeks, and 1 week later (starting from the 2nd week) they were injected with DOX (2.5 mg/kg BW i.p.) every other day for 2 weeks. Rats treated with DOX alone exhibited notable myocardial damage (discontinuity and disorganization of cardiac muscle fibers, mononuclear cell infiltration, and apparent increases in collagen fiber deposition) accompanied by loss of function (revealed by elevated serum levels of lactate dehydrogenase, creatine kinase, and cardiac troponin), induction of oxidative stress (indicated by higher levels of nitric oxide and malondialdehyde, and lower levels of superoxide dismutase, catalase, and glutathione peroxidase), apoptosis (evidenced by high caspase 3 activity and immunostaining), and inflammation (marked by high cardiac NFκB level). However, administration of CAR not only ameliorated all deleterious effects of DOX but also induced angiogenesis, as indicated by a significant increase in VEGF immunoreactivity. These data indicate that CAR could relieve DOX-induced cardiotoxicity, at least in part, via reductions in oxidative stress, apoptosis, and inflammation and increased tissue regeneration via induction of angiogenesis. Therefore, CAR could be a promising cytoprotective agent against DOX cardiotoxicity.

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“…ESTA was neither cytotoxic by itself nor an enhancer of DOX cytotoxicity, rather, administration of ESTA allowed an approximately five-fold reduction in dose of DOX to achieve equal therapeutic effect perhaps through the indirect effect of suppressing the DOX treatment-associated T H 2 shift. Anthracycline-induced cardiomyopathy, including oxidative stress [23][24][25], IL-1-mediated inflammation [23,[26][27][28], and cardiac apoptosis [23,24], limits the allowable cumulative lifetime dose; thus, reduction of DOX dosage while maintaining efficacy is an attractive therapeutic strategy. ESTA blocked de novo infiltration of CD45 + cells and the T H 2 shift in the DOX-treated tumors; however, the effect of DOX/ESTA on other ogans remains unaddressed.…”

Section: Discussionmentioning

confidence: 99%

“…Theoretically, blockade of tissue infiltration of immune cells is attainable through targeting a 268 key mediator in the adhesion cascade (i.e., immune cells, cytokines/chemokines, or vessels). Thus 269 far, immune cells (α4 integrin [23] or CD11b/CD18 [24]) and chemokines (macrophage colony…”

Section: Esta Suppressed T H 2-related Pro-tumorgenic Changesmentioning

confidence: 99%

Functional Blockade of E-Selectin in Tumor-Associated Vessels Enhances Anti-Tumor Effect of Doxorubicin in Breast Cancer

Morita

Leslie

Kameyama

et al. 2020

Cancers

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Chemotherapy is a mainstay of treatment for solid tumors. However, little is known about how therapy-induced immune cell infiltration may affect therapy response. We found substantial CD45 + immune cell density adjacent to E-selectin expressing inflamed vessels in doxorubicin (DOX)-treated residual human breast tumors. While CD45 level was significantly elevated in DOX-treated wildtype mice, it remained unchanged in DOX-treated tumors from E-selectin null mice. Similarly, intravenous administration of anti-E-selectin aptamer (ESTA) resulted in a significant reduction in CD45 + immune cell density in DOX-treated residual tumors, which coincided with a delay in tumor growth and lung metastasis in MMTV-pyMT mice. Additionally, both tumor infiltrating T-lymphocytes and tumor associated-macrophages were skewed towards T H 2 in DOX-treated residual breast tumors; however, ESTA suppressed these changes. This study suggests that DOX treatment instigates de novo intratumoral infiltration of immune cells through E-selectin, and functional blockade of E-selectin may reduce residual tumor burden as well as metastasis through suppression of T H 2 shift.

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Allicin ameliorates doxorubicin-induced cardiotoxicity in rats via suppression of oxidative stress, inflammation and apoptosis

Abstract: The current study demonstrated that allicin effectively mitigates cardiac oxidative damage, apoptosis and inflammation, induced by acute DOX intoxication. Therefore, allicin could be a promising cytoprotective agent against DOX cardiotoxicity.

Cited by 132 publications

References 52 publications

Cardiotoxicity and myocardial infarction‐associated DNA damage induced by thiamethoxam in vitro and in vivo: Protective role of Trigonella foenum‐graecum seed‐derived polysaccharide

Cardiotoxicity and myocardial infarction‐associated DNA damage induced by thiamethoxam in vitro and in vivo: Protective role of Trigonella foenum‐graecum seed‐derived polysaccharide

Ameliorative Effect of Cardamom Aqueous Extract on Doxorubicin-Induced Cardiotoxicity in Rats

Functional Blockade of E-Selectin in Tumor-Associated Vessels Enhances Anti-Tumor Effect of Doxorubicin in Breast Cancer

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