Ameliorative effect of parsley oil on cisplatin-induced hepato-cardiotoxicity: A biochemical, histopathological, and immunohistochemical study

Abdellatief, Suhair A.; Galal, Azza A.A.; Farouk, Sameh Mohamed; Abdel-Daim, Mohamed M.

doi:10.1016/j.biopha.2016.12.038

Cited by 87 publications

(54 citation statements)

References 37 publications

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“…Although the accurate mechanism of CP-induced nephrotoxicity is not well understood, previous study suggested that cisplatin interacts with DNA, through the formation of covalent adducts between certain DNA bases and the platinum compound leading to cell cytotoxicity [49]. Other studies suggest that CP-induced ROS and immune response which are mediators of nephrotoxicity [50–52]. In the present study, the MDA and GSH were measured as biomarkers for the oxidative stress.…”

Section: Discussionmentioning

confidence: 70%

Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

et al. 2017

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BackgroundCisplatin (CP) is commonly used in the treatment of different types of cancer but nephrotoxicity has been a major limiting factor. Therefore, the present study aimed to study the possible protective effect of rutin against nephrotoxicity induced by cisplatin in rats.MethodsForty male Wistar albino rats were randomly divided into 4 groups. Rats of group 1 control group intraperitoneal (i.p.) received 2.5 ml/kg, group 2 CP group received single dose 5 mg/kg cisplatin i.p. group 3 rutin group orally received 30 mg/kg rutin group 4 (CP plus rutin) received CP and rutin as in group 2 and 3. Kidneys were harvested for histopathology and for the study the gene expression of c-Jun N-terminal kinases (JNK), Mitogen-activated protein kinase 4 (MKK4), MKK7, P38 mitogen-activated protein kinases (P38), tumor necrosis factors alpha (TNF-α), TNF Receptor-Associated Factor 2 (TRAF2), and interleukin-1 alpha (IL-1-α).ResultsThe cisplatin single dose administration to rats induced nephrotoxicity associated with a significant increase in blood urea nitrogen (BUN) and serum creatinine and significantly increase Malondialdehyde (MDA) in kidney tissues by 230 ± 5.5 nmol/g compared to control group. The animal treated with cisplatin showed a significant increase in the expression levels of the IL-1α (260%), TRFA2 (491%), P38 (410%), MKK4 (263%), MKK7 (412%), JNK (680%) and TNF-α (300%) genes compared to control group. Additionally, histopathological examination showed that cisplatin-induced interstitial congestion, focal mononuclear cell inflammatory, cell infiltrate, acute tubular injury with reactive atypia and apoptotic cells. Rutin administration attenuated cisplatin-induced alteration in gene expression and structural and functional changes in the kidney. Additionally, histopathological examination of kidney tissues confirmed gene expression data.ConclusionThe present study suggested that the anti-oxidant and anti-inflammatory effect of rutin may prevent CP-induced nephrotoxicity via decreasing the oxidative stress, inhibiting the interconnected ROS/JNK/TNF/P38 MAPK signaling pathways, and repairing the histopathological changes against cisplatin administration.

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Section: Discussionmentioning

confidence: 70%

Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

et al. 2017

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“…The continuous use of chemical inputs such as pesticides has resulted in great damage to the environment in addition to human ill‐health. The clinical impact of pesticides is marked by an increasing risk of myocardial injury and congestive heart failure, chiefly caused by reactive oxygen species generation . However, many studies have reported the benefits of medicinal plants in the treatment of cardiovascular diseases due to their richness in bioactive compounds.…”

Section: Discussionmentioning

confidence: 99%

“…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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“…The occurrence of congenital heart disease is attributed to many factors, such as genetic factors, environmental factors, pathogenic microorganism infections, and drug toxicity, among which the drug toxicity played an important role in cardiac development defects (18). For example, tilmicosin (19), doxorubicin (20), cisplatin (21) and diclofenac sodium (21) have been previously reported to induce cardiotoxicity by regulating oxidative stress. However, the teratogenicity and cardiotoxicity of isoniazid on fetal heart development was still rarely reported.…”

Section: Introductionmentioning

confidence: 99%

Isoniazid causes heart looping disorder of zebrafish embryo by inducing oxidative stress

Wang¹,

Liu²,

Wei³

et al. 2019

Preprint

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The cardiotoxicity of isoniazid on zebrafish embryos and its underlying mechanism remained unclear. Here, we exposed zebrafish embryos at 4 hours post fertilization to different levels of isoniazid and recorded the morphology and number of malformed and dead embryos under the microscope. The high concentration of isoniazid group showed more malformed and dead embryos compared with low dose of isoniazid group and control group. Besides, the morphology of heart and its alteration were visualized using the transgenic zebrafish (cmlc2: GFP) and confirmed by in situ hybridization. The negative effects of isoniazid on the developing heart were characterized by lower heart rate and more heart looping disorders. Mechanistically, PCR showed decreased expression of heart-specific transcription factors exposed to isoniazid. Oxidative stress was induced by Isoniazid in cardiomyocytes, mediated by decreased activity of CAT and SOD, which could be rescued by ROS scavenger. In conclusion, we demonstrated that isoniazid lead to heart looping disturbance by downregulating cardiac specific transcription factors and inducing cardiomyocytes apoptosis.

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Ameliorative effect of parsley oil on cisplatin-induced hepato-cardiotoxicity: A biochemical, histopathological, and immunohistochemical study

Cited by 87 publications

References 37 publications

Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

Protective effect of rutin supplementation against cisplatin-induced Nephrotoxicity in rats

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

Isoniazid causes heart looping disorder of zebrafish embryo by inducing oxidative stress

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