Protective role of silymarin and D-penicillamine against lead-induced liver toxicity and oxidative stress

2017 ◽  
Vol 33 (6) ◽  
pp. 512-518 ◽  
Author(s):  
Seyedeh Missagh Jalali ◽  
Hossein Najafzadeh ◽  
Sadegh Bahmei
Keyword(s):  
Liver Toxicity ◽  
Serum Alkaline Phosphatase ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Antioxidant Defence ◽  
Antioxidant Defence System ◽  
Pb Exposure ◽  
Group 2

This study was performed to assess hepatotoxicity and alterations in liver antioxidant defence in acute lead (Pb) exposure and the protective effects of silymarin in comparison to D-penicillamine in rats. Forty eight Albino rats were divided in eight groups and received the following treatments in a 10-day experiment – group 1: normal saline as control; group 2: 25-mg/kg Pb acetate, intraperitoneally (IP) for the last 5 days; group 3: 100-mg/kg D-penicillamine, IP for the last 5 days; group 4: 200-mg/kg silymarin, orally for 10 days; and groups 5, 6, 7 and 8: in addition to Pb, they received D-penicillamine, for the last 5 days, silymarin for 10 days, a combination of silymarin for 10 days and D-penicillamine for the last 5 days and silymarin for the last 5 days, respectively. Pb acetate exposure induced significant elevation in serum alkaline phosphatase (ALP), aspartate aminotransferase (AST) and alanine aminotransferase (ALT) enzyme activities in group 2 compared to control group. Significant reductions in serum total protein and albumin in all Pb-exposed groups and in serum glucose in groups 2, 6 and 8 were also observed. Liver tissue superoxide dismutase and glutathione peroxidase were significantly lower in groups 2 and 8 compared to control group. Silymarin pretreatment and D-penicillamine administration in groups 5, 7 and 8 could significantly lower ALP, ALT and AST and improve liver antioxidant enzymes. Thus, acute Pb exposure induced hepatotoxicity with suppression of liver antioxidant defence system and silymarin, as an antioxidant could alleviate this effect.

Effects of erdosteine on cyclosporin-A-induced nephrotoxicity

2011 ◽  
Vol 31 (6) ◽  
pp. 565-573 ◽  
Author(s):  
M Tutanc ◽  
V Arica ◽  
N Yılmaz ◽  
A Nacar ◽  
I Zararsiz ◽  
...  
Keyword(s):  
Oxidative Stress ◽  
Cyclosporin A ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Protective Mechanism ◽  
Antioxidant Parameters ◽  
Group 2 ◽  
Wistar Albino Rats

Aim: In cyclosporin-A (CsA)-induced toxicity, oxidative stress has been implicated as a potential responsible mechanism. Therefore, we aimed to investigate the protective role of erdosteine against CsA-induced nephrotoxicity in terms of tissue oxidant/antioxidant parameters and light microscopy in rats. Materials and methods: Wistar albino rats were randomly separated into four groups. Group 1 rats treated with sodium chloride served as the control, group 2 rats were treated with CsA, group 3 with CsA plus erdosteine, and group 4 with erdosteine alone. Animals were killed and blood samples were analyzed for blood urea nitrogen (BUN), serum creatinine (Cr), uric acid (UA), total protein (TP), and albumin (ALB) levels. Kidney sections were analyzed for malondialdehyde (MDA) and nitric oxide (NO) levels and superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities, as well as for histopathological changes. Results: In the CsA group, MDA, GSH-Px, BUN, and Cr levels were increased. The TP and ALB levels were decreased. These changes had been improved by erdosteine administration. Other biochemical parameters did not show any significant change. Conclusion: These results indicate that erdosteine produces a protective mechanism against CsA-induced nephrotoxicity and suggest a role of oxidative stress in pathogenesis.

scholarly journals Antioxidant Effect of MnTE-2-PyP on Lung in Asthma Mice Model

2012 ◽  
Vol 2012 ◽  
pp. 1-6 ◽  
Author(s):  
Lyudmil Terziev ◽  
Violeta Dancheva ◽  
Veneta Shopova ◽  
Galya Stavreva
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Control Group ◽  
Mice Model ◽  
Antioxidant Defence ◽  
Group 4 ◽  
Antioxidant Defence System ◽  
Group 3 ◽  
Group 2 ◽  
Group 1

Aim. To investigate the effects of MnTE-2-PyP on some markers of antioxidant defence system in asthma mice model.Material and Methods. The animals were divided into four groups: group 1, controls; group 2, injected with ovalbumin, group 3, treated with MnTE-2-PyP, and group 4, treated with ovalbumin and MnTE-2-PyP. The activities of superoxide dismutase, catalase, glutathione peroxidase and nonprotein sulfhydryl groups content (NPSH) were determined in lung homogenate.Results. The activities of superoxide dismutase and catalase in group 2 decreased significantly as compared to control group. The decrease of the same enzymes in group 4 was lower and significant as compared to group 2. Changes in the glutathione peroxidase activity showed a similar dynamics. The NPSH groups content decreased in group 2. In group 4 this decrease was relatively lower as compared to group 2.Conclusions. The application of MnTE-2-PyP mitigated the effects of oxidative stress in asthma mice model.

scholarly journals Chlorogenic and Caftaric Acids in Liver Toxicity and Oxidative Stress Induced by Methamphetamine

2014 ◽  
Vol 2014 ◽  
pp. 1-10 ◽  
Author(s):  
Khaled M. M. Koriem ◽  
Rowan E. Soliman
Keyword(s):  
Oxidative Stress ◽  
Chlorogenic Acid ◽  
Liver Toxicity ◽  
Density Lipoprotein ◽  
Acute Hepatic Failure ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Dietary Polyphenols ◽  
And Oxidative Stress

Methamphetamine intoxication can cause acute hepatic failure. Chlorogenic and caftaric acids are the major dietary polyphenols present in various foods. The aim of this study was to evaluate the protective role of chlorogenic and caftaric acids in liver toxicity and oxidative stress induced by methamphetamine in rats. Thirty-two male albino rats were divided into 4 equal groups. Group 1, which was control group, was injected (i.p) with saline (1 mL/kg) twice a day over seven-day period. Groups 2, 3, and 4 were injected (i.p) with methamphetamine (10 mg/kg) twice a day over seven-day period, where groups 3 and 4 were injected (i.p) with 60 mg/kg chlorogenic acid and 40 mg/kg caftaric acid, respectively, one day before methamphetamine injections. Methamphetamine increased serum aspartate aminotransferase, alanine aminotransferase, alkaline phosphatase, bilirubin, cholesterol, low-density lipoprotein, and triglycerides. Also, malondialdehyde in serum, liver, and brain and plasma and liver nitric oxide levels were increased while methamphetamine induced a significant decrease in serum total protein, albumin, globulin, albumin/globulin ratio, brain serotonin, norepinephrine and dopamine, blood and liver superoxide dismutase, and glutathione peroxidase levels. Chlorogenic and caftaric acids prior to methamphetamine injections restored all the above parameters to normal values. In conclusion, chlorogenic and caftaric acids before methamphetamine injections prevented liver toxicity and oxidative stress where chlorogenic acid was more effective.

The protective role of curcumin against toxic effect of nonylphenol on bone development

2021 ◽  
pp. 096032712110305
Author(s):  
P Alısan Suna ◽  
O Cengız ◽  
A Ceyhan ◽  
E Atay ◽  
T Ertekin ◽  
...  
Keyword(s):  
Toxic Effect ◽  
Corn Oil ◽  
Bone Development ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Wistar Albino Rats ◽  
The Sacrifice

Introduction: In the study, it was aimed to investigate the possible protective effects of curcumin, a potent antioxidant, against the toxic effect of nonylphenol on bone development. Methods: Thirty pregnant female Wistar albino rats were used. The rats were randomly divided into the following five groups; the control group, corn oil group (150 µl/kg/day), nonylphenol group (50 µl/kg/day), curcumin group (100 mg/kg/day) and curcumin + nonylphenol group (100 mg/kg/day + 50 µl/kg/day). The doses were given by gavage from the 5th day to the 20th day of gestation. The fetuses were removed out on the 20th day of pregnancy by cesarean at the end of the study. After the sacrifice of the animals, double skeletal staining in front extremity (clavicula, scapula, humerus, radius, ulna) and hind extremity (femur, tibia, fibula), additionally histological and immunohistochemical examinations in femur bone were performed. Results: The nonylphenol group offspring have the lowest weights of fetuses and placenta, head-to-hip lengths, biparietal and occipitofrontal length, and also, bone length percentage and percentage of the ossification area in all measurements of the front extremity and hind extremity Interestingly, the groups treated with curcumin showed close to the control group in terms of double skeletal staining, histological, and immunohistochemical examinations. Conclusions: Our findings demonstrated an association between bone development and exposure to nonylphenol. The findings suggest that curcumin treatments may be effective in accelerating bone formation.

Protective effects of combined β-caryophyllene and silymarin against ketoprofen-induced hepatotoxicity in rats

2016 ◽  
Vol 94 (7) ◽  
pp. 739-744 ◽  
Author(s):  
Mohamed Elsayed Kelany ◽  
Mohamed Abdelmohsen Abdallah
Keyword(s):  
Antioxidant Capacity ◽  
Total Antioxidant Capacity ◽  
Liver Toxicity ◽  
Treated Group ◽  
Control Group ◽  
Albino Rats ◽  
Distilled Water ◽  
Protective Effects ◽  
Total Antioxidant ◽  
Liver Changes

Ketoprofen (Ket), widely utilized in treatment of many inflammatory disorders, is found to induce liver toxicity especially with overdose. This study aimed to evaluate the possible protective effects of concomitant β-caryophyllene (Cary) and silymarin (Sily) against Ket-induced hepatotoxicity in rats. Forty adult male albino rats were divided into 5 groups (each n = 8): the control group received distilled water for 6 weeks; the Ket-treated group received distilled water for 5 weeks and Ket in a dose of 8 mg·kg−1·day−1 p.o. for the 6th week; the Cary + Ket treated group received Cary in a dose of 200 mg·kg−1·day−1 orally for 6 weeks and Ket for the 6th week; the Sily + Ket treated group received Sily in the dose of 150 mg·kg−1·day−1 for 6 weeks and Ket for the 6th week; and the Cary + Sily + Ket treated group received Sily and Cary for 6 weeks and Ket for the 6th week. At end of the experiment, serum ALT, AST, and albumin and liver total antioxidant capacity (t.TAC) and malondialdehyde (t.MDA) were measured in all rats. Ket increased serum ALT and AST and t.MDA and decreased t.TAC. Cary and Sily improved these changes. Combined Cary and Sily restored these liver changes to nearly normal. Combined Cary and Sily is hepatoprotective, with the ability to scavenge oxidants against Ket-induced hepatotoxicity in rats.

scholarly journals Triazophos induced neuro-splenic toxicity and evaluation of antioxidative potential of aqueous Broccoli extract in Wistar albino rats

2021 ◽  
Vol 13 (2) ◽  
pp. 616-626
Author(s):  
Dharmender Sharma ◽  
Gurinder Kaur Sangha
Keyword(s):  
Histological Study ◽  
Control Group ◽  
Albino Rats ◽  
White Pulp ◽  
Protective Effects ◽  
Glutathione S Transferase ◽  
Group 4 ◽  
Group 5 ◽  
Group 2 ◽  
Wistar Albino Rats

The present investigation was carried out to assess the antioxidative potential of Broccoli sprouts aqueous extract (BE) against triazophos (TZ) induced oxidative stress (OS) in brain and spleen. In the experimental setup, six groups of rats were formed; Control (group 1), BE (group 2), TZ (group 3), and also BE+TZ groups such as BE1 (group 4), BE2 (group 5) and BE3 (group 6) groups. Rats were orally intubated for 30 days as per experimental design. After sacrifice, OS biomarkers viz; catalase (CAT), superoxide dismutase (SOD), glutathione reductase (GR), glutathione peroxidase (GPx), glutathione-S-transferase (GST), and lipid peroxidation (LPO) levels were determined in brain and spleen. Acetylcholinesterase (AChE) activity was observed in plasma and brain samples. Histological study of the spleen in TZ rats showed increased thickness of capsule, congestion and hypocellularity in follicles of spleen’s white pulp and the histoarchitecture was restored in TZ+BE group rats. TZ caused degenerative changes in brain histology and rats showed mild congestion along with haemorrhage in the cerebral cortex. Results suggest that TZ exposure is associated with neural toxicity along with altered spleen stress biomarkers, which further corroborates with histopathological findings. It is inferred that BE exerts multi-mechanistic protective effects against TZ induced neuro-splenic toxicity which is attributable to its protective antioxidant actions.

scholarly journals THE PROTECTIVE EFFECT OF THE CARTHMUS TINCTORIUS LEAVES EXTRACTON METHOTREXATE-INDUCED PULMONARY FIBROSIS IN RATS

2019 ◽  
pp. 89-92
Author(s):  
HANAA SALMAN KHADHEM ◽  
MAHDI MTHUWAINI ◽  
WAJDY J. MAJID
Keyword(s):  
Pulmonary Fibrosis ◽  
Histopathological Examination ◽  
Relative Weight ◽  
Carthamus Tinctorius ◽  
Protective Role ◽  
Control Group ◽  
Albino Rats ◽  
Lung Weight ◽  
Group 2

Objective: Pulmonary fibrosis (PF) is an irreversible and untreatable human disease encompasses a large group of chronic lung disorders associated with excessive remodeling, scarring, and fibrosis. The current work was designed to study the harmful effects of methotrexate (MTX) administration on the lung and the possible protective role of Carthmus tinctorius leaves extract. The animals were utilized in this study. Methods: A total of 40 male healthy adult Wistar albino rats with anaverage body weight of 200±25 g, were divided into four groups (10 animals each). G1: control group, G2: MTX group, G3: Carthamus tinctorius (CT), group G4:MTX+Carthamus tinctorius(CT). CT was administered orally at a dose of (40 mg/kg/day) for 4 w to G3 and G4. The (CT) group were performed to explore any toxic effect of the (CT) extract on the lung. Rats of G2 and G4 administered 4 mg/kg dose of MTX orally for 28 d. Rats of G1 were intraperitoneally (i. p) administered with normal saline 0.5 ml ∕ day for four weeks (4wk) to serveas control. The animals were weighed at the beginning, though, and at the end of experiments. Results: The study showed that the relative lung weight was significantly increased at (P˂0.01) in MTX-treated animals in comparison to the control group. A combination of CT extract with MTX revealed significant decrease (P<0.01) in the lung relative weight in comparison to MTX group. Histopathological examination revealed that lung injury was less severe in group 3 and 4compared to group 2. The results indicated that CT significantly decreased collagen deposition, hydroxyproline content, and ameliorated pathological changes. Conclusion: The study has clearly identified the importance protective role of CT extract on pulmonary fibrosis induced by methoxerate. We recommended CT as one of therapeutic strategy to amelioratethe lung fibrosis associated with methotrexate therapy.

scholarly journals Doxorubicin-Induced Cardio Toxicity in Albino Rats Protected by Adansonia Digitata (Baobab) Leaf Extract

2021 ◽  
pp. 12-22
Author(s):  
Akintola Adebola Olayemi ◽  
Kehinde Busuyi David ◽  
Saka Waheed Adeoye ◽  
Oyewande Esther Ajoke ◽  
Ayandiran Tolulope Akinpelu ◽  
...  
Keyword(s):  
Cardiovascular Disease ◽  
Leaf Extract ◽  
Myocardial Damage ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Adansonia Digitata ◽  
Group 2 ◽  
Doxorubicin Group ◽  
Myocardial Infection

Cardiovascular disease is the world's leading cause of death, killing 17 to 19 million people each year. The usage of traditional drugs was influenced by the need for effective medications for the treatment of cardiovascular disease without side effects. The current study investigated the cardio-protective effects of Adansonia digitata leaf extract on doxorubicin-mediated cardiotoxicity in laboratory rats. Thirty-five albino rats were divided into five groups, each consisting of seven rats. Group 1 was given filtered water as a control, while Group 2 was given saline and doxorubicin, Group 3 received doxorubicin and Vitamin E, and Groups IV and V were myocardial oxidative animals treated with Adansonia digitata leaf extract (150 and 300 mg/kg/wt) for two weeks. After the rats were sacrificed, their hearts were collected and homogenized for biochemical assays. The results on the activities of creatinine kinase (CK), lactate dehydrogenase (LDH), aspartate amino transferase (AST), nitric oxide synthase (NOS), superoxide dismutase (SOD), catalase (CAT), and malondialdehyde were determined. Histopathology examination was used in addition to assays to validate myocardial damage. In comparison to the control group, rats provided doxorubicin showed a significant increase in the activities of cardiac marker enzymes (CK, LDH, and AST), as well as a significant increase in malondialdehyde concentration with a concomitant decrease in antioxidant enzymes (SOD, CAT, and NOS), implying cardiotoxicity. In rats with doxorubicin-induced myocardial infection, pretreatment with Adansonia digitata leaf extract reduced myocardial damage, these biochemical results were confirmed by histopathology. Finally, the new study demonstrates that Adansonia digitata has cardioprotective properties.

scholarly journals Hepatoprotective effect of galangin on carbon tetrachloride-induced hepatotoxicity via the LKB1/AMPK pathway

2021 ◽  
Vol 19 ◽  
pp. 205873922110008
Author(s):  
Meng Chen ◽  
Xinyan Song ◽  
Jifang Jiang ◽  
Lei Xing ◽  
Pengfei Wang
Keyword(s):  
Carbon Tetrachloride ◽  
Liver Toxicity ◽  
Corn Oil ◽  
Histopathological Examination ◽  
Hepatoprotective Effect ◽  
Control Group ◽  
Group Model ◽  
Protective Effects ◽  
Model Group ◽  
Expression Levels

To investigate the protective effects of galangin on liver toxicity induced by carbon tetrachloride (CCl4) in mice. Mouse hepatotoxicity model was established by intraperitoneal injection (i.p.) of 10 ml/kg body weight CCl4 that diluted with corn oil to a proportion of 1:500 on Kunming mice. The mice were randomly divided into five groups named control group, model group, and 1, 5, and 10 mg/kg galangin group. The levels of alanine aminotransferase (ALT) and aspartate aminotransferase (AST) were analyzed by ELISA. Liver histopathological examination was observed via optical microscopy. The levels of superoxide dismutase (SOD), malondialdehyde (MDA), glutathione (GSH), and glutathion (GSSG) were analyzed to assess oxidative stress. Finally, western blot assay was carried out to analyse the expression levels of total AMP-activated protein kinase (AMPK), phospho-AMPK (p-AMPK), total liver kinase B1 (LKB1), and phospho-LKB1 (p-LKB1). Compared with the control group, in the model group, the levels of AST, ALT, MDA, and GSSG increased significantly ( p < 0.01); the activity of SOD and GSH decreased significantly ( p < 0.01); and the histopathological examination revealed liver necrosis. However, treatment with galangin (5 and 10 mg/kg) significantly reversed these CCl4-induced liver damage indicators. Furthermore, treatment with galangin (10 mg/kg) significantly increased the p-AMPK and p-LKB1 expression levels ( p < 0.01). This study supports the hepatoprotective effect of galangin against hepatotoxicity, perhaps occurring mainly through the LKB1/AMPK-mediated pathway.

scholarly journals Probucol Attenuates Cyclophosphamide-induced Oxidative Apoptosis, p53 and Bax Signal Expression in Rat Cardiac Tissues

2010 ◽  
Vol 3 (5) ◽  
pp. 308-316 ◽  
Author(s):  
Yousif A. Asiri
Keyword(s):  
Superoxide Dismutase ◽  
Glutathione Peroxidase ◽  
Mrna Expression ◽  
Corn Oil ◽  
Lipid Lowering ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Antioxidant Genes ◽  
Cardiac Tissues

Cyclophosphamide (CP) is a widely used drug in cancer chemotherapy and immunosuppression, which could cause toxicity of the normal cells due to its toxic metabolites. Probucol, a cholesterol-lowering drug, acts as potential inhibitor of DNA damage and shows to protect against doxorubicin-induced cardiomyopathy by enhancing the endogenous antioxidant system including glutathione peroxidase, catalase and superoxide dismutase. This study examined the possible protective effects of probucol, a lipid-lowering compound with strong antioxidant properties, against CPinduced cardiotoxicity. This objective could be achieved through studying the gene expression-based on the possible protective effects of probucol against CP-induced cardiac failure in rats. Adult male Wistar albino rats were assigned into four treatment groups: Animals in the first (control) and second (probucol) groups were injected intraperitoneally with corn oil and probucol (61 mg/kg/day), respectively, for two weeks. Animals in the third (CP) and fourth (probucol plus CP) groups were injected with the same doses of corn oil and probucol (61 mg/kg/day), respectively, for one week before and one week after a single dose of CP (200 mg/kg, I.P.). The p53, Bax, Bcl2 and oxidative genes signal expression were measured by real time PCR. CP-induced cardiotoxicity was clearly observed by a significant increase in serum creatine phosphokinase isoenzyme (CK-MB) (117%), lactate dehydrogenase (LDH) (64%), free (69%) and esterified cholesterol (42%) and triglyceride (69%) compared to control group. In cardiac tissues, CP significantly increases the mRNA expression levels of apoptotic genes, p53 with two-fold and Bax with 1.6-fold, and decreases the anti-apoptotic gene Bcl2 with 0.5-fold. Moreover, CP caused downregulation of antioxidant genes, glutathione peroxidase, catalase, and superoxide dismutase and increased the lipid peroxidation and decreased adenosine triphosphate (ATP) (40%) and ATP/ADP (44%) in cardiac tissues. Probucol pretreatment not only counteracted significantly the CP-induced increase in cardiac enzymes and apoptosis but also induced a significant increase in mRNA expression of antioxidant enzymes and improved ATP, ATP/ADP, glutathione (GSH) in cardiac tissues. In conclusion, data from the present study suggest that probucol prevents the development of CP-induced cardiotoxicity by a mechanism related, at least in part, to its ability to increase mRNA expression of antioxidant genes and to decrease apoptosis in cardiac tissues with the consequent improvement in mitochondrial oxidative phosphorylation and energy production.

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