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

2018 ◽  
Vol 206 (1-2) ◽  
pp. 62-72 ◽  
Author(s):  
Maha Abu Gazia ◽  
Mohammed Abu El-Magd
Keyword(s):  
Oxidative Stress ◽  
Elevated Serum ◽  
Myocardial Damage ◽  
Serum Levels ◽  
Control Group ◽  
Albino Rats ◽  
Loss Of Function ◽  
Group I ◽  
Ameliorative Effect ◽  
Fiber Deposition

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.

scholarly journals Effects of l-Carnitine on the Follicle-Stimulating Hormone, Luteinizing Hormone, Testosterone, and Testicular Tissue Oxidative Stress Levels in Streptozotocin-Induced Diabetic Rats

2018 ◽  
Vol 23 ◽  
pp. 2515690X1879605 ◽  
Author(s):  
Nourollah Rezaei ◽  
Tahereh Mardanshahi ◽  
Majid Malekzadeh Shafaroudi ◽  
Saeed Abedian ◽  
Hamid Mohammadi ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Luteinizing Hormone ◽  
Follicle Stimulating Hormone ◽  
Serum Levels ◽  
Diabetic Rats ◽  
Diabetic Group ◽  
Control Group ◽  
Group Vi ◽  
Group I ◽  
Stimulating Hormone

The present study was designed to investigate the antioxidant property of l-carnitine (LC) on serum levels of follicle-stimulating hormone (FSH), luteinizing hormone (LH), testosterone (TH) and testis oxidative stress in streptozotocin (STZ)-induced diabetic rats. The rats were divided into the following groups: group I, control; group II, LC 100 mg/kg/d; group III, diabetic; and groups IV to VI, diabetic rats treated with 50, 100, and 200 mg/kg/d of LC, respectively. Daily injections were given intraperitoneally for 7 weeks. At the end of experimental period, after sacrificing the rats, FSH, LH, TH, total antioxidant capacity (TAC), malondialdehyde (MDA), glutathione (GSH), catalase (CAT), mitochondrial function (MTT), protein carbonyl (PC), and reactive oxygen species (ROS) levels were measured. STZ caused an elevation of MDA, ROS, and PC ( P < .001) with reduction of GSH, CAT, TAC, and MTT ( P < .001) in the serum levels. Group VI had significantly increased FSH, LH, and TH levels versus the untreated diabetic group ( P < .001). Although groups V and VI significantly decreased MDA ( P < .001), PC ( P < .01), and ROS ( P < .01) compared with the untreated diabetic group; only in group VI, the activity of GSH ( P < .001), CAT ( P < .01), TAC ( P < .001), and MTT ( P < .001) significantly increased. The results of the present study suggest that LC decreased diabetes-induced oxidative stress complications and also improved serum level of FSH, LH, and TH by reducing levels of lipid peroxidation and increasing antioxidant enzymes.

The Antioxidant Efficacy of Wheatgrass (Triticum Aestivum) on Mercuric Chloride (HgCl2) - Induced Oxidative Stress in Rat Model

2021 ◽  
Vol 9 (2) ◽  
pp. 450-464
Author(s):  
Renu Tripathi ◽  
Swati Agarwal ◽  
Syed Ibrahim Rizvi ◽  
Neetu * Mishra
Keyword(s):  
Oxidative Stress ◽  
Mercuric Chloride ◽  
Rat Model ◽  
Antioxidant Status ◽  
Protective Efficacy ◽  
Density Lipoprotein ◽  
Control Group ◽  
Albino Rats ◽  
Antioxidant Power ◽  
Group I

Mercury is a harmful toxic pollutant, which has hepato-nephrotoxic, hematotoxic, genotoxic and neurotoxic, effects. The aim of the study was to evaluate the protective efficacy of wheatgrass on mercuric chloride (HgCl2) induced oxidative stress and associated complications in rat model. Albino rats were divided into four groups (three rats per group). Group I normal control group. Group II oxidative stressed group received mercuric chloride (0.5 mg/kg/day). Group III only received wheatgrass extract (100 mg/kg/day), whereas Group IV received wheatgrass (100 mg/kg/day) after one hour, followed by mercuric chloride (0.5 mg/kg/day) for 30 days. The results of the study showed that wheatgrass supplementation significantly decreased the HgCl2 induced elevated oxidative stress parameters Plasma Malondialdehyde (MDA) content, Plasma membrane redox system (PMRS), Advanced oxidation protein products (AOPP), simultaneously elevated lipid profile (Total Cholesterol, Triglycerides, Low-density lipoprotein (LDL), liver enzymes as, Plasma Alkaline phosphatase (ALP), Aspartate aminotransferase (AST), and Alanine aminotransferase (ALT), Serum Urea, and Creatinine levels in rats. In addition, wheatgrass treatment improved the antioxidant status in terms of intracellular Reduced Glutathione (GSH), Ferric reducing antioxidant power (FRAP) and 2, 2- diphenyl -1- picrylhydrazyl (DPPH). Therefore it can be concluded that wheatgrass has great potential to diminish the stress-mediated complications and improve the antioxidant status.

scholarly journals The Effects of Hyperbaric Oxygen at Different Pressures on Oxidative Stress and Antioxidant Status in Rats

Medicina ◽  
2019 ◽  
Vol 55 (5) ◽  
pp. 205 ◽  
Author(s):  
Şefika Körpınar ◽  
Hafize Uzun
Keyword(s):  
Oxidative Stress ◽  
Hyperbaric Oxygen ◽  
Antioxidant Status ◽  
Central Retinal Artery Occlusion ◽  
Retinal Artery Occlusion ◽  
Antioxidant Response ◽  
Control Group ◽  
Albino Rats ◽  
Normobaric Oxygen ◽  
Group I

Background: The optimal use of oxygen at greater than atmospheric pressures in any operational or therapeutic application (hyperbaric oxygen, HBO2) requires awareness of the fact that the beneficial effects of oxygen coexist with toxic effects depending on the pressure and duration of exposure. In this study, we aimed to investigate the effect of HBO2 therapy on oxidative stress and antioxidant status in commonly used protocol for acute HBO2 indications, such as carbon monoxide intoxication, central retinal artery occlusion, crush injury, gas gangrene, and to compare it with normobaric oxygen (NBO2) in healthy rats. Materials and Methods: Fifty-six male, young adult Wistar albino rats were randomly divided into seven groups and named as Group I through Group VII. Plasma malondialdehyde (MDA), superoxide dismutase (SOD), and erythrocyte glutathione (GSH) levels in control group were compared to the levels in other groups. Results: The increases in MDA levels and the decrease in SOD activities were statistically significant in HBO2 groups at the end of the first 24 h when compared to the control group, and the significant decrease in erythrocyte GSH level was only at 2.4 atmospheres absolute. Conclusions: The present study showed that pressure and frequency of exposure are important factors to consider when investigating HBO2-induced oxidative stress and antioxidant response.

scholarly journals Possible Protective Effect of Silver Nanoparticles against Cisplatin Induced Pulmonary Inflammation in Rat Model

2021 ◽  
pp. 453-463
Author(s):  
Hanan Y. Alharbi ◽  
Nawal W. Helmi ◽  
Neveen A. Salem
Keyword(s):  
Oxidative Stress ◽  
Silver Nanoparticles ◽  
Lung Tissue ◽  
Pulmonary Inflammation ◽  
Normal Lung ◽  
Control Group ◽  
Albino Rats ◽  
Dependent Manner ◽  
Apoptotic Markers ◽  
Group I

Silver nanoparticles (AgNPs) are gaining interest in medical applications for their prominent antibacterial and antimicrobial potentials. AgNPs possess remarkable anti-inflammatory and antioxidant activities and enhances wound healing. The main objective of the current study was to investigate the therapeutic effect of administration of AgNPs on cisplatin (CP) induced pulmonary inflammation in rats. Sixty male albino rats were used in this study. Rats were divided into 6 groups (n=10). Group I control group. Group II and III control groups received AgNPs at doses (5 and 10 ppm). Group IV CP group received CP (2.5 mg/kg). Group V and VI CP group received AgNPs (5, and 10 ppm). All doses were administered intraperitoneally once a day for 4 weeks. Oxidative stress and antioxidant status, inflammatory mediators, fibrogenic as well as apoptotic markers were determined in lung tissues. The results revealed that rats treated with CP showed remarkable elevation in lung tissues MDA, TNF-α, IFN-γ, IL-6, CRP, Fibrinogen and P53 levels associated with depression in SOD, GSH and CAT activities. However, administration of AgNPs (5 or 10 ppm) to CP group resulted in significant amelioration of the aforementioned parameters in a dose dependent manner. Histopathological investigation of lung tissues of CP group demonstrated disruption of normal lung architecture and lung injury. However, treatment with AgNPs revealed significant improvement in lung tissue against CP- induced inflammatory changes and lung tissue damage. It could be concluded that AgNPs exert potent cytoprotective effects via combating oxidative stress, inflammation, fibrogenic and apoptotic markers and repairing histopathological changes in lung tissues.

scholarly journals Glutathione ameliorates liver markers, oxidative stress and inflammatory indices in rats with renal ischemia reperfusion injury

2018 ◽  
Vol 8 (2) ◽  
pp. 91-97 ◽  
Author(s):  
Hassan Ahmadvand ◽  
Esmaeel Babaeenezhad ◽  
Maryam Nasri ◽  
Leila Jafaripour ◽  
Reza Mohammadrezaei Khorramabadi
Keyword(s):  
Oxidative Stress ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Serum Levels ◽  
Renal Ischemia ◽  
Paraoxonase 1 ◽  
Pon1 Activity ◽  
Control Group ◽  
Group I ◽  
Liver Markers

Introduction: Glutathione (GSH) protects the tissue and cell from oxidative injury. Objectives: In the current study, we investigated the possible effects of GSH on liver markers, oxidative stress and inflammatory indices in rat with renal ischemia reperfusion (RIR) injury. Materials and Methods: Twenty-four adult male Wistar rats were divided into 3 groups (n=8). Group I (the control group), group II (the RIR group) received saline (0.25 mL/d, intraperitoneally; i.p.), group III as the RIR group that received GSH (100 mg/kg/d, i.p.). The treatment with saline or GSH began daily 14 days before RIR induction. RIR was induced by clamping renal pedicles for 45 minutes and 24 hours of reperfusion. Results: RIR significantly increased the serum level of nitric oxide (NO), the serum activities of aspartate aminotransferase (AST), alkaline phosphatase (ALP), gamma-glutamyltransferase (GGT), the serum and renal levels of malondialdehyde (MDA), and the serum activity of myeloperoxidase (MPO). However, RIR significantly decreased the serum and renal levels of GSH, serum paraoxonase 1 (PON1) activity, and the serum and renal activities of catalase (CAT) and glutathione peroxidase (GPX). GSH administration could significantly improve the serum activities of AST, GGT, MPO, GPX and PON1 and serum levels of NO, renal MDA, GSH levels, and serum and also renal CAT activities. Conclusion: Our study indicated that GSH administration ameliorated RIR injury in rats by improving the activities of liver markers and antioxidant enzymes, the levels of MDA, NO, GSH and MPO activity.

Ameliorative effect of curcumin against tamoxifen in-duced hepatotoxicity in female albino rats

2017 ◽  
Vol 2 (2) ◽  
pp. 223-239
Author(s):  
Saber A. Sakr ◽  
Hoda A. Mahran ◽  
Hagar A. Abu Quora
Keyword(s):  
Body Weight ◽  
Dose Level ◽  
Biochemical Markers ◽  
Antioxidant Activities ◽  
Control Group ◽  
Albino Rats ◽  
Bile Duct Proliferation ◽  
Leukocytic Infiltration ◽  
Group I ◽  
Ameliorative Effect

The objective of the present work was to investigate the ameliorative effect of curcumin (Cur) against tamoxifen (TAM), a nonsteriodal antiestrogenic drug, induced hepatotoxicity in adult female albino rats. Forty eight female albino rats were divided into four groups of equal size. groups: group (I) animals of this group were served as control, group (II) rats were orally given Cur at a dose level of 150 mg/kg body weight daily for nine weeks, group (III) rats were orally given TAM at a dose level of 20 mg/kg body weight daily for nine weeks and group (IV) rats were given TAM followed by Cur at the same previous doses daily for nine weeks. For histological and immunohistochemical studies, livers were immediately removed after sacrification and sera were collected to detect the biochemical markers. Liver sections of rats treated with TAM showed loss of the normal architecture, cytoplasmic vacuolation, leukocytic infiltration and bile duct proliferation as well as increase in the expression of both alpha smooth muscle actin (α-SMA) and Ki-67. The activities of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) and the level of malondialdehyde (MDA) were elevated, while the activities of catalase (CAT), superoxide dismutase (SOD) and the level of glutathione (GSH) were decreased in sera of rats of TAM group. On the other hand, liver sections of rats treated with TAM followed by Cur showed improvement in the histological, immunohistochemical and the biochemical markers. In conclusion, Cur revealed ameliorative effect against TAM toxicity in rat liver due to its antioxidant activities.

In vivo effects of intravenous lipid emulsion on lung tissue in an experimental model of acute malathion intoxication

2018 ◽  
Vol 34 (2) ◽  
pp. 110-118 ◽  
Author(s):  
Murat Uysal ◽  
Serhat Karaman
Keyword(s):  
Oxidative Stress ◽  
Lung Tissue ◽  
Lipid Emulsion ◽  
Caspase 3 ◽  
Control Group ◽  
Albino Rats ◽  
Sod Activity ◽  
Expression Levels ◽  
Intravenous Lipid Emulsion ◽  
Group I

Malathion can be ingested, inhaled, or absorbed through the skin, but acute toxicity is maximized when administered orally. Intravenous lipid emulsion (ILE) treatment is used as a new therapeutic method in cases of systemic toxicity caused by some lipid soluble agents. This study aimed to examine the potential treatment effect of ILE on rat lung tissue in a toxicokinetic model of malathion exposure. Twenty-one adult Wistar albino rats were randomly divided into three equal groups. The groups were organized as group I (control), group II (malathion), and group III (malathion + ILE treatment). Malondialdehyde (MDA), superoxide dismutase (SOD), and glutathione peroxidase (GSH-Px) were evaluated in lung tissues. Immunohistochemical and Western blot analyses were performed to determine the bax, bcl-2, and caspase-3 expression levels. Tissue GSH-Px and SOD activities were decreased and MDA levels were increased in the malathion group. ILE administration increased GSH-Px and SOD activity and decreased MDA levels compared to the malathion group. Furthermore, expression of bax, bcl-2, and caspase-3 significantly increased in the malathion group, and ILE infusion reduced these expression levels. The present study revealed that acute oral malathion administration increased oxidative stress and apoptosis in the lung tissue of rats. ILE infusion prevented oxidative stress and decreased the deleterious effects of malathion. Taken together, the findings of our study suggest that lipid emulsion infusion has treatment efficacy on malathion-induced lung toxicity.

scholarly journals Sinapic Acid Ameliorates Oxidative Stress, Inflammation, and Apoptosis in Acute Doxorubicin-Induced Cardiotoxicity via the NF-κB-Mediated Pathway

2020 ◽  
Vol 2020 ◽  
pp. 1-10 ◽  
Author(s):  
Yousef A. Bin Jardan ◽  
Mushtaq Ahmad Ansari ◽  
Mohammad Raish ◽  
Khalid M. Alkharfy ◽  
Abdul Ahad ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Cardiac Tissue ◽  
Interleukin 1 ◽  
Sinapic Acid ◽  
Serum Levels ◽  
Daily Administration ◽  
Control Group ◽  
Group I ◽  
Male Wistar Rats

In the present study, we explored SA’s activity against DOX-induced cardiotoxicity and revealed its underlying mechanisms. Male Wistar rats (weight, 190-210g; n=6) were randomly divided into four groups: group I, normal control; group II, DOX 15 mg/kg via intraperitoneal (ip) route; group III, administered DOX+SA 20 mg/kg; and group IV, administered DOX+captopril (CAP 30 mg/kg). SA and CAP were administered orally for seven days, and DOX (15 mg/kg) was injected intraperitoneally an hour before SA treatment on the fifth day. Forty-eight hours after DOX administration, animals were anesthetized and sacrificed for molecular and histology experiments. SA significantly mitigated the myocardial effects of DOX, and following daily administration, it reduced serum levels of lactate dehydrogenase (LDH) and creatine kinase isoenzyme-MB to near normal values. Levels of oxidative stress markers, glutathione-peroxidase, superoxide dismutase, and catalase, in the cardiac tissue were significantly increased, whereas malondialdehyde levels decreased after SA treatment in DOX-administered rats. Furthermore, DOX caused an inflammatory reaction by elevating the levels of proinflammatory cytokines, tumor necrosis factor-α (TNF-α), interleukin-1β (IL-1β), and endothelin- (ET-) 1, as well as nuclear factor kappa-B (NF-κB) expression. Daily administration of SA significantly repressed TNF-α, IL-1β, ET-1, and NF-κB levels. caspase-3 and Bax expression, bcl-2-like protein and caspase-3 activities and levels. Overall, we found that SA could inhibit DOX-induced cardiotoxicity by inhibiting oxidative stress, inflammation, and apoptotic damage.

Vitamin D attenuates gentamicin-induced acute renal damage via prevention of oxidative stress and DNA damage

2018 ◽  
Vol 38 (3) ◽  
pp. 321-335 ◽  
Author(s):  
MA Mohammed ◽  
BE Aboulhoda ◽  
RH Mahmoud
Keyword(s):  
Oxidative Stress ◽  
Vitamin D ◽  
Dna Damage ◽  
Kidney Function ◽  
Control Group ◽  
Albino Rats ◽  
Nuclear Factor ◽  
Group I ◽  
First Choice ◽  
Depth Analysis

Background: Despite being one of the most nephrotoxic drugs, gentamicin (GM) remains a mainstay as a first-choice agent in a vast variety of clinical situations owing to its superlative efficiency as a broad-spectrum antibiotic in treating several life-threatening bacterial infections. This urgently calls for the need for in-depth analysis of the mechanisms governing GM-induced nephrotoxicity and entails the necessity of presenting novel protective agents capable of ameliorating those renal deleterious effects. The reactive oxygen species and redox-sensitive transcription factors in GM-induced nephrotoxicity have recently called attention. Purpose: This study has been designed to shed light on the possible mechanisms of GM-induced nephrotoxicity and to provide a consensus set of histopathological, immunohistochemical, genetic and biochemical parameters elucidating the protective role of vitamin D against this nephrotoxicity. Methods: Twenty-four adult male albino rats were equally divided into four groups: group I (control group), group II (GM), group III (GM + vitamin D) and group IV (vitamin D only). Kidney function tests, histopathological examination, gene expression of nuclear factor 2, nuclear factor kappa beta (NF-κB) and western blot of NF-κB p65, assessment of glutathione peroxidase and nicotinamide adenine dinucleotide phosphate oxidase (NADPH) oxidase by ELISA, as well as immunohistochemical evaluation of inducible nitric oxide, malondialdehyde, 8-hydroxy 2 deoxyguanine and vitamin D receptor, have been carried out. Results: The kidney function deterioration, tissue oxidative stress development and the histopathological changes induced by GM were significantly attenuated by vitamin D administration. Conclusion: Vitamin D attenuates GM nephrotoxicity through its antioxidant properties and prevention of DNA damage.

Effect of pycnogenol and spirulina on vancomycin-induced renal cortical oxidative stress, apoptosis, and autophagy in adult male albino rat

2016 ◽  
Vol 94 (8) ◽  
pp. 838-848 ◽  
Author(s):  
Naglaa A. Bayomy ◽  
Eman Z. Abdelaziz ◽  
Mona A. Said ◽  
Marwa S. Badawi ◽  
Reda H. El-Bakary
Keyword(s):  
Oxidative Stress ◽  
Morphological Changes ◽  
Elevated Serum ◽  
Natural Antioxidants ◽  
Control Group ◽  
Protective Effects ◽  
Drug Induced ◽  
Albino Rat ◽  
Group I ◽  
Vancomycin Group

Vancomycin-induced nephrotoxicity has been reported to occur in 5%–25% of patients who were administered with it. Several natural antioxidants were found to be effective against drug-induced toxicity. We evaluated the possible protective effects of spirulina and pycnogenol alone or in combination on vancomycin-induced renal cortical oxidative stress. Forty-nine rats were randomly divided into 7 groups: group I, control; group II, received spirulina 1000 mg/kg per day; group III, received pycnogenol 200 mg/kg per day; group IV, received vancomycin 200 mg/kg per day every 12 h; group V, (spirulina + vancomycin); group VI, (pycnogenol + vancomycin); and group VII, (pycnogenol + spirulina + vancomycin). At the end of the experiment, kidney functions were estimated and then the kidneys were removed, weighed, and sampled for histopathological, immunohistochemistry, and biochemical studies. Administration of spirulina and pycnogenol alone or in combination decreased elevated serum creatinine, blood urea nitrogen, renal malondialdehyde, and immunoexpression of the proapoptotic protein (Bax), autophagic marker protein (LC3/B), and inducible nitric oxide synthase induced by vancomycin. They increased reduced glutathione, glutathione peroxidase, superoxide dismutase, and immunoexpression of the antiapoptotic protein (Bcl2). They also ameliorated the morphological changes induced by vancomycin. The combination therapy of spirulina and pycnogenol showed better protective effects than the corresponding monotherapy.

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