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 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.

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 A Novel Role of SIRT1/ FGF-21 in Taurine Protection Against Cafeteria Diet-Induced Steatohepatitis in Rats

2017 ◽  
Vol 43 (2) ◽  
pp. 644-659 ◽  
Author(s):  
Azza H. Abd Elwahab ◽  
Basma K. Ramadan ◽  
Mona F. Schaalan  ◽  
Amina M. Tolba
Keyword(s):  
Caspase 3 ◽  
B Cell Lymphoma ◽  
Cafeteria Diet ◽  
Control Group ◽  
Albino Rats ◽  
Protective Mechanism ◽  
Alcoholic Fatty Liver ◽  
Group I ◽  
Tnf Α

Background: Non-alcoholic fatty liver disease (NAFLD) is one of the alarmingly rising clinical problems in the 21st century with no effective drug treatment until now. Taurine is an essential amino acid in humans that proved efficacy as a non-pharmacological therapy in a plethora of diseases; however, its impact on NAFLD remains elusive. The aim of the current study is to evaluate the protective mechanism of taurine in experimental steatohepatitis induced by junk food given as cafeteria-diet (CAF-D) in male albino rats. Methods: Forty adult male albino rats of local strain between 8-10 weeks old, weighing 150 ± 20 g, were divided into four equal groups: Group I (control group), Group II (Taurine group), Group III (CAF-D for 12 weeks) and Group IV (CAF-D +Taurine). CAF-D was given in addition to the standard chow for 12 weeks, where each rat was given one piece of beef burger fried in 15 g of sunflower oil, one teaspoonful of mayonnaise, and one piece of petit pan bread, weighing 60g/ piece. In the serum, liver function tests; ALT, AST, ALP, GGT and the lipid profile; TG, TC, HDL-C added to reduced glutathione (GSH) were assessed colorimetrically, while fibroblast growth factor (FGF)-21, adiponectin & interleukin (IL)-6 via ELISA. The same technique was used for the assays of the hepatic levels of FGF-21, silent information regulator (SIRT1), malondialdehyde (MDA),IL-10, tumor necrosis factor-α (TNF-α) as well as the apoptotic markers; caspase-3 and B-cell lymphoma (Bcl-2). Results: The cafeteria-diet induced steatohepatitis was reflected by significantly increased body and liver weight gain, elevation of liver enzymes; ALT, AST, ALP and GGT added to the dyslipidemic panel, presented as increased TC, TG, LDL-C and decreased HDL-C levels. The steatosis-induced inflammatory milieu, marked by elevated serum levels of FGF-21, IL-6, hepatic TNF-α, as well as reduced IL-10 and adiponectin, was associated with steatosis- induced hepatic oxidative stress, reflected by increased hepatic MDA and decreased GSH levels, along with stimulated caspase-3 and decline in BcL-2 hepatic levels. These pathological disturbances were significantly ameliorated by taurine supplementation and evidenced histopathologically. The cross talk between hepatic FGF-21 and SIRT1 and their association to the induced perturbations are novel findings in this study. Taurine's efficacy in restoration of hepatic structure and function is partially via the increase in SIRT1 and associated reduction of FGF-21. Conclusion: The findings of the current study prove the protective role of taurine in NAFLD via a novel role in the amelioration of FGF-21/ SIRT1 axis, which could be considered a new therapeutic target.

Redox and apoptotic potential of novel ruthenium complexes in the rat blood and heart

2020 ◽  
Author(s):  
Katarina Mihajlovic ◽  
Isidora Milosavljevic ◽  
Jovana Jeremic ◽  
Maja Savic ◽  
Jasmina Sretenovic ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Caspase 3 ◽  
Ruthenium Complexes ◽  
Redox Status ◽  
Heart Tissue ◽  
Control Group ◽  
Albino Rats ◽  
Oxidative Stress Biomarkers ◽  
Tissue Samples ◽  
Relative Expression

Ruthenium(II) complexes offer the potential for lower toxicity compared to platinum(II) complexes. Our study aimed to compare cardiotoxicity of [Ru(Cl-tpy)(en)Cl][Cl], [Ru(Cl-tpy)(dach)Cl][Cl], [Ru(Cl-tpy)(bpy)Cl][Cl], cisplatin and saline through assessment of redox status and relative expression of apoptosis-related genes. A total of 40 Wistar albino rats were divided into five groups. Ruthenium groups received intraperitoneally single dose of complexes (4 mg/kg/week) for 4-weeks period; cisplatin group received cisplatin (4 mg/kg/week) and control group received saline (4 mL/kg/week) in the same manner as ruthenium groups. In collected blood and heart tissue samples, spectrophotometrically determination of oxidative stress biomarkers was performed. The relative expression of apoptosis-related genes (Bcl-2, Bax, and caspase-3) in hearts was examined by RT-PCR. Our results showed that systemic and cardiac pro-oxidative markers (TBARS and NO2-) were significantly lower in ruthenium groups compared to cisplatin group, while concentrations of antioxidative parameters (CAT, SOD, and GSSG) were significantly higher. Ruthenium administration led to significantly lower gene expression of Bax and caspase-3 compared to cisplatin-treated rats, while Bcl-2 remained unchanged. Applied ruthenium complexes have less pronounced potential for induction of oxidative stress-mediated cardiotoxicity compared to cisplatin. These findings may help for future studies that should clarify the mechanisms of cardiotoxicity of ruthenium-based metallodrugs.

Effects of selenium, zinc, insulin and metallothionein on cadmium-induced oxidative stress and metallothionein gene expression levels in diabetic rats

2020 ◽  
Vol 31 (2) ◽  
Author(s):  
Huseyin Gungor ◽  
Haki Kara
Keyword(s):  
Oxidative Stress ◽  
Gene Expression ◽  
Diabetic Rats ◽  
Control Group ◽  
Activity Levels ◽  
Sod Activity ◽  
Expression Levels ◽  
Group 6 ◽  
Group 5 ◽  
Gene Expression Levels

AbstractBackgroundThe aim of this study was to investigate the effects of selenium, zinc, insulin, and metallothionein on oxidative damage and metallothionein (MT) gene expression levels in streptozotocin (STZ)-induced type 1 diabetic rats exposed to Cd.MethodsRats were categorized under eight groups (control, STZ, Cd, STZ + Cd, Group 5, Group 6, Group 7, and STZ + Cd + MT [n:8/group]) were used. After diabetes was induced by STZ (55 mg/kg, i.p.), Cd was administered (1 mg/kg CdCl, orally) for 4 weeks. In cadmium-treated groups selenium (Na2SeO3 1.5 mg/kg, i.p.), zinc (ZnSO4 10 mg/kg via oral gavage), insulin (insulin glargine, 2U/day, s.c.), and MT (1mg/kg, every other 10 days, s.c.) were administered. MT gene expression levels, MDA levels, GPx, SOD, and CAT activity levels were determined in liver and kidney tissues.ResultsMT gene expression and MDA levels increased (p < 0.05) while GPx and SOD activity levels decreased (p < 0.05) in STZ, Cd, and STZ + Cd groups. In Group 5, Group 6, Group 7, and Group 8 groups MT gene expression and MDA levels were decreased while GPx and SOD activity levels were increased (p < 0.05). CAT activity significantly increased (p < 0.05) in STZ + Cd group while there were no significance in other groups (p > 0.05). Compared to the control, Group 5, Group 6, Group 7, and Group 8 groups provided no difference for alanine aminotransferase, aspartate aminotransferase, blood urea nitrogen and creatinine levels (p > 0.05).ConclusionsOur results suggest that Se, insulin, Zn and MT may have protective effects against hepatotoxicity and nephrotoxicity caused by Cd exposure in diabetic rats by reducing oxidative stress and MT gene expression levels.

Pregabalin Ameliorates Lipopolysaccharide-Induced Pancreatic Inflammation in Aged Rats

2019 ◽  
Vol 19 (8) ◽  
pp. 1141-1147 ◽  
Author(s):  
Ozlem Ozmen ◽  
Senay Topsakal
Keyword(s):  
Caspase 3 ◽  
Pancreatic Tissue ◽  
Control Group ◽  
Albino Rats ◽  
Histopathological Analysis ◽  
Aged Rats ◽  
Tissue Samples ◽  
Glucose Levels ◽  
Amyloid A ◽  
Group I

Objective: The aim of this study was to examine pancreatic pathology and the prophylactic effects of pregabalin in lipopolysaccharide (LPS) induced sepsis model in aged rats. Methods: Twenty-four female, one-year-old, Wistar Albino rats were assigned to three groups; Group I (control), Group II (study group: 5mg/kg LPS intraperitoneal, single dose) and Group III(treatment group: 5mg/kg LPS+30 mg/kg oral pregabalin one hour before LPS). Animals were sacrificed by exsanguination 6 hours after LPS administration. Blood and pancreatic tissue samples were collected for biochemical, pathological, and immunohistochemical analyses. Results: LPS caused increases in serum amylase and lipase level but led to a reduction in glucose levels. Following histopathological analysis, numerous neutrophil leucocyte infiltrations were observed in vessels and pancreatic tissues. Increased caspase-3 expression was observed in both the endocrine and exocrine pancreas in the LPS group. Similarly, IL-6, caspase-3 (Cas-3), inducible nitric oxide synthase (iNOS), granulocyte colony-stimulating factor (G-CSF) and serum amyloid-A (SAA) expressions were increased by LPS. Pregabalin improved biochemical, histopathological, and immunohistochemical findings. Conclusion: This study showed that LPS causes pathological findings in the pancreas, but pregabalin has ameliorative effects in aged rats with sepsis. Cas-3, IL-6, iNOS, G-CSF, and SAA all play pivotal roles in the pathogenesis of LPS-induced pancreatic damage.

Sufentanil Affects High Glucose-Induced Oxidative Stress in and Apoptosis of Cardiomyocytes by Regulation of miR-142-3p Expression

2021 ◽  
Vol 11 (3) ◽  
pp. 466-470
Author(s):  
Zhiyong Liu ◽  
Cuiqing Ding ◽  
Changqing Yao ◽  
Jinhui Chen
Keyword(s):  
Oxidative Stress ◽  
High Glucose ◽  
Molecular Mechanisms ◽  
Caspase 3 ◽  
Control Group ◽  
High Dose ◽  
Dependent Manner ◽  
Sod Activity ◽  
Apoptosis Rate ◽  
Mda Content

To explore the effects and molecular mechanisms of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes, cardiomyocytes H9c2 cells were classified into groups based on different treatments as high-glucose (HG), HG with low, medium, or high-dose sufentanil, HG with high-dose sufentanil and anti-miR-NC, HG with high-dose sufentanil and anti-miR-142-3p, and control. The cells’ superoxide dismutase (SOD) activity and malondialdehyde (MDA) content were detected using respective kits. The apoptosis rate in each group was detected by flow cytometry. The expressions of cleaved caspase-3 and pro-caspase3 were determined using western blotting. The expression of miR-142-3p in cardiomyocytes was detected using real-time fluorescent quantitative PCR. Compared with the control group, the HG group had decreased SOD activity, pro-caspase-3 expression, and miR-142-3p expression and increased MDA content, apoptosis, and cleaved caspase-3 expression (P < 0.05). Compared with the HG group, the SOD activity and pro-caspase-3 expression increased and the MDA content, apoptosis rate, and cleaved caspase-3 expression decreased in HG cells treated with low, medium, or high-dose sufentanil. The expression of miR-142-3p was increased in a dose-dependent manner (P < 0.05). The interference of miR-142-3p reversed the effect of sufentanil on high glucose-induced oxidative stress in and apoptosis of cardiomyocytes. Sufentanil may inhibit high glucose-induced oxidative stress in and apoptosis of cardiomyocytes by upregulating miR-142-3p expression.

Effect of Mir-663 on the Differentiation of Bone Marrow Mesenchymal Stem Cells in Inflammatory Environment Through Regulating Oxidative Stress and Transforming Growth Factor β1

2019 ◽  
Vol 9 (11) ◽  
pp. 1600-1606
Author(s):  
Xiuhong Sun ◽  
Yujie Liu ◽  
Shujuan Zheng
Keyword(s):  
Oxidative Stress ◽  
Real Time ◽  
Real Time Pcr ◽  
Caspase 3 ◽  
Transforming Growth Factor ◽  
Transforming Growth Factor Β1 ◽  
Control Group ◽  
Sod Activity ◽  
Alp Activity ◽  
Marrow Mesenchymal Stem Cells

BMSCs are beneficial for the treatment of Osteoarthritis (OA). Mir-663 involves in various diseases. However, the role of Mir-663 in the differentiation of BMSCs in an inflammatory environment remains unclear. Rat BMSCs were isolated and divided into control group, and inflammation group which was treated with 1 μg/ml lipopolysaccharide (LPS), Mir-663 group and Mir-663 siRNA groups which was respectively transfected with Mir-663 plasmid and Mir-663 siRNA into LPS-treated BMSCs followed by analysis of the survival rate of BMSC by MTT, Caspase 3 activity, ALP activity, expression of osteogenic genes Runx2 and OP by Real time PCR, ROS content and SOD activity, TGF-β1 level by Real time PCR and ELISA, TNF- and IL-1 secretion by ELISA. LPS treatment significantly increased Mir-663 expression, inhibited cell proliferation, increased Caspase 3 activity, and inhibited ALP activity. Meanwhile it also significantly decreased Runx2 and OP expression, increased ROS content, decreased SOD activity and TGF-β1 expression as well as elevated TNF-α and IL-1β secretion compared to control (P < 0.05); Mir-663 plasmid transfection can further promote the above changes (P < 0.05); whereas, Mir-663 siRNA could reverse the above changes (P < 0.05). Mir-663 expression was increased in BMSCs in inflammatory environment. Down-regulation of Mir663 expression can regulate oxidative stress, up-regulate TGF-β1 level, inhibit the secretion of TNF-α and IL-1β, and promote the proliferation and osteogenic differentiation of BMSCs in inflammatory environment.

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.

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