scholarly journals Evaluation of protective effects of melatonin on free radical metabolism in rat kidney during ischemia-reperfusion

2019 ◽  
pp. 20-29
Author(s):  
M. Nisari ◽  
A. Yay ◽  
T. Ertekin ◽  
M. Nisari ◽  
Ö. Al ◽  
...  
Keyword(s):  
Tap Water ◽  
Rat Kidney ◽  
Ischemia Reperfusion ◽  
Oxidant Stress ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Sod Activity ◽  
Renal Pedicle ◽  
Group I

The purpose of this research was to investigate the possible protective effect of melatonin, as a potent antioxidant on I/R-induced renal injury in rats. Methods. We used 28 female Wistar albino rats weight 200-250g. The rats were randomly divided into 4 groups. Control Group (C): They were fed with only standard rat diet and tap water without drug injections or ischemia-reperfusion. Melatonin Group (M): 25 mg/kg melatonin was administered i.p 30 min.  Ischemia/Reperfusion Group (I/R): Rats were subjected to 45 min of renal pedicle occlusion followed by 24 hours reperfusion. Melatonin+ischemia/reperfusion Group (M+I/R): Melatonin (25 mg/kg) was administered 30 min prior to ischemia and immediately before the reperfusion period. Rats were subjected to 45 min of renal pedicle occlusion followed by 24 hours reperfusion. Results. While MDA levels increased in the I/R group, SOD and GST activities were seen to be significantly increased. Although the increase of the SOD activity was observed in the M+I/R group, no meaningful difference was found. MDA levels were significantly decreased in M+I/R group compared to the control group, CAT and GST activities were significantly increased. Conclusions. Our results show that the treatment with M may prevent kidney damage due to ischemia result in increasing oxidant stress peroxidation damages further. Melatonin or its metabolites are capable of neutralizing free radicals and non-radical oxygen-based reactants. This study suggests that melatonin may be an effective antioxidant agent.

scholarly journals Protective Effects of Selenium Against Sodium Fluoride Induced Behavioral, Anti-Oxidant and Neurohistological Alterations in Wistar Rats

2018 ◽  
Vol 15 (2) ◽  
pp. 475-484 ◽  
Author(s):  
Gorantla Sri Charitha ◽  
Kurmeti Sudhakar ◽  
K. Pratap Reddy
Keyword(s):  
Sodium Fluoride ◽  
Wistar Rats ◽  
Motor Coordination ◽  
Soft Tissues ◽  
Tap Water ◽  
Control Group ◽  
Protective Effects ◽  
Sod Activity ◽  
Group I ◽  
Anti Oxidant

Fluoride naturally occurs in the earth’s crust and ground water and it causes fluorosis when it is consumed in high levels. The fluorosis also affects soft tissues like liver, kidney, heart, brain etc., in addition to skeletal and dental systems. The present study reports the protective effects of selenium against sodium fluoride induced neurotoxic effects. Three months old (around 250 – 280 g weight) wistar rats were randomly categorized into four groups viz. Group I (control) which received normal tap water, Group II (sodium fluoride, NaF) treated with 20 ppm of fluoride through IP, Group III treated with (NaF 20 ppm) + Selenium (5 mgkg-1 body wt./day/rat) and Group IV treated with Selenium (5 mgkg-1 body wt./day/rat) alone. The doses were continued for a period of 15 days and after that they were used for recording behavioral (rota rod, hot plate), anti-oxidant (LPO, SOD, CAT and GSH-Px) and histological (Golgi cox staining) observations. The rats treated with NaF showed the decreased motor coordination, thermal pain response, decreased CAT and SOD activity and increased LPO levels and GSH-Px activity with compared to control group. Moreover, NaF received rats also showed the decreased number of dendrites, synaptic connections and neural networks. These all alterations were reversed on administration of selenium towards fluoride toxicity and the results were significant (p<0.01). The results of selenium alone treated group of rats is comparable to control group. Based on these observed results, the present study evidenced the protective role of selenium against fluoride induced neurotoxicity.

scholarly journals Protective effects of tempol in an experimental ovarian ischemia–reperfusion injury model in female Wistar albino rats

2017 ◽  
Vol 95 (7) ◽  
pp. 861-865 ◽  
Author(s):  
Neslihan Pınar ◽  
Oya Soylu Karapınar ◽  
Oğuzhan Özcan ◽  
Esin Atik Doğan ◽  
Suphi Bayraktar
Keyword(s):  
Sham Group ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Stress Index ◽  
Albino Rats ◽  
Protective Effects ◽  
Group V ◽  
Group Iii ◽  
Group I ◽  
Wistar Albino Rats

The aim of this study was to investigate the antioxidant effects of tempol on ovarian ischemia–reperfusion (I/R) injury in rats. Forty female Wistar albino rats were randomly divided into 5 groups: Group I, sham; Group II, ischemia (I); Group III, I/R; Group IV, I/R + tempol 30 mg/kg i.p; Group V, I/R + tempol 50 mg/kg i.p. Oxidative stress index (OSI) was significantly higher in the ischemia group and the I/R group than in the sham group. Catalase levels were significantly lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. Glutathione peroxidase levels were lower in the I/R group than in the I/R + tempol 30 mg/kg i.p. and the I/R + tempol 50 mg/kg i.p. groups. MDA levels were significantly lower in the I/R + tempol 30 mg/kg i.p. group and the I/R + tempol 50 mg/kg i.p. group than in the I/R group. The levels of the histopathological parameters were significantly decreased in the I/R + tempol 50 mg/kg i.p. group compared with the I/R group. Tempol can be used for reducing ovarian I/R injury.

Protective effect of N-acetylcysteine, caffeic acid and vitamin E on doxorubicin hepatotoxicity

2007 ◽  
Vol 26 (6) ◽  
pp. 519-525 ◽  
Author(s):  
A. Gokcimen ◽  
A. Cim ◽  
H.T. Tola ◽  
D. Bayram ◽  
A. Kocak ◽  
...  
Keyword(s):  
Vitamin E ◽  
Caffeic Acid ◽  
Control Group ◽  
Albino Rats ◽  
Central Vein ◽  
Protective Effects ◽  
Injection Group ◽  
Hepatocellular Damage ◽  
Group I ◽  
Significant Difference

The aim of this study was to compare the possible protective effects of N-acetylcysteine (NAC), caffeic acid (CAPE) and vitamin E (Vit-E) on doxorubicin-induced hepatotoxicity. Thirty-two male Wistar albino rats, weighing between 250 and 350 g were supplied and randomly divided into five groups. Animals in study groups were pretreated with a single dose of doxorubicin (Dox), which was administered intraperitoneally (i.p.). Control group (Group I) was treated with intraperitoneal saline injection. Group II did not received any antioxidant agent after the injection. Group III and Group IV were given CAPE and intraperitoneal vitamin E injection for eight days, respectively. Group V received NAC for eight days. The study was finished after 10 days. Tissue samples were collected from all animals and histopathological examination was performed. There was statistically significant difference between the experiment groups and controls by means of mononuclear cell infiltration and diameters of hepatic sinusoid, terminal hepatic venule (central vein) and portal area (portal canal). Changes related with hepatocellular damage were more prominent, whereas there was no significant difference between Dox and NAC given groups histopathologically. It was observed that structural changes were regressed after CAPE administration. However, this recovery was more prominent in vitamin E given group. These findings suggest that Dox induced liver damage could be efficiently reversed by vitamin E administration. It has been found that CAPE, but not NAC has protective effects on Dox-induced hepatocellular damage. Human & Experimental Toxicology (2007) 26, 519—525

scholarly journals Effects of Cilostazol and Diltiazem Hydrochloride on Ischemia-Reperfusion Injury in a Rat Hindlimb Model

2017 ◽  
Vol 20 (2) ◽  
pp. 058 ◽  
Author(s):  
Bekir İNAN ◽  
Selma SÖNMEZ ERGÜN ◽  
Asiye NURTEN ◽  
Canan KÜÇÜKGERGİN ◽  
Aslı ZENGİN TÜRKMEN ◽  
...  
Keyword(s):  
Reperfusion Injury ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Saline Group ◽  
Dimethyl Sulphoxide ◽  
Control Group ◽  
Albino Rats ◽  
Diltiazem Hydrochloride ◽  
Beneficial Effects ◽  
Group I

Objective: Free radicals and neutrophils are potent sources of ischemia-reperfusion injury (I/R) and they can be limited by the use of exogenous application of some therapeutic agents. The objective of this study was to compare the effects of cilostazol and diltiazem hydrochloride in a rat hind limb model of I/R injury. Methods: Skeletal muscles submitted to 2 hours of ischemia by placing an aneurysm clip to femoral artery and reperfused after 1, 2 and 4 hours. Seventy-two Wistar-Albino rats were randomly divided into mainly four groups according to treatment agents:  Group I (control group) was treated with saline; Group II was treated with diltiazem hydrochloride; Group III was treated with cilostazol in 30% dimethyl sulphoxide; and Group IV was treated with 30% dimethyl sulphoxide intraperitoneally. These four main groups also subdivided into three subgroups according to duration of the reperfusion times.  Blood samples were taken and all rats were sacrificed. Results: Cilostazol-treated groups demonstrated a significant decrease in tissue and serum malondialdehyde (MDA) levels, and tissue myeloperoxidase (MPO ) activity compared with other groups. Increase in serum nitric oxide (NOx) level was significantly higher in all subgroups of cilastazol, diltiazem hydrochloride, and dimethyl sulphoxide groups versus the control group.Conclusion: Although these results suggest the beneficial effects of cilostazol and diltiazem hydrochloride on I/R injury, the effect of cilostazol on I/R injury seems to be more efficient than diltiazem hydrochloride.

Protective effects of olmesartan and l-carnitine on doxorubicin-induced cardiotoxicity in rats

2020 ◽  
Vol 98 (4) ◽  
pp. 183-193 ◽  
Author(s):  
Malek M. Aziz ◽  
Mai A. Abd El Fattah ◽  
Kawkab A. Ahmed ◽  
Helmy M. Sayed
Keyword(s):  
Transforming Growth Factor Beta ◽  
Troponin I ◽  
Transforming Growth Factor ◽  
Antineoplastic Agent ◽  
The Other ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Group I ◽  
Creatine Kinase Mb

Doxorubicin (DOX), an anthracycline antibiotic, is an important antineoplastic agent due to its high antitumor efficacy in hematological as well as in solid malignancies. The clinical use of DOX is limited due to its cardiotoxic effects. The present study aimed to investigate the possible protective effect of olmesartan (Olm), l-carnitine (L-CA), and their combination in cardiotoxicity induced by DOX in rats. Male albino rats were randomly divided into seven experimental groups (n = 8): group I: normal control, group II: L-CA, group III: Olm, group IV: DOX. The other three groups were treated with Olm (10 mg/kg), L-CA (300 mg/kg), and their combination for 2 weeks after induction of cardiotoxicity by a single dose of DOX (20 mg/kg). In the results, DOX showed a significant elevation in serum troponin I, creatine kinase-MB (CK-MB), and lactate dehydrogenase (LDH) together with increased inflammation manifested by the rise of tumor necrosis factor-alpha (TNF-α), intercellular adhesion molecules-1 (ICAM-1), interleukin IL-1β (IL-1β), myeloperoxidase (MPO), nuclear factor-kappa B (NF-κB), and transforming growth factor beta (TGF-β) in cardiac tissues as well as DOX-induced oxidative stress by increasing in malondialdehyde (MDA) and decreasing in superoxide dismutase (SOD) and glutathione (GSH) in heart tissues. In addition, caspase-3 activity was boosted as indication of increased apoptosis. On the other hand, administration of L-CA and Olm attenuated the DOX-evoked disturbances in the abovementioned parameters. In addition, DOX exhibited echocardiographic changes and severe histopathological changes, which were significantly reversed by L-CA and Olm treatment. In conclusion, the present study data confirm the protective role of L-CA and Olm in DOX-induced cardiotoxicity, which may be related to its antioxidant, antiinflammatory, and antiapoptotic agents.

scholarly journals Antioxidant Properties and Protective Effect of Aqueous Anti-Ulcer Drug (AQAUD) against Aspirin-induced Gastric Ulcers in Albino Rats

2020 ◽  
pp. 9-21
Author(s):  
B. A. Mba ◽  
C. S. Alisi ◽  
A. C. Ene
Keyword(s):  
Protective Effect ◽  
Antioxidant Properties ◽  
Toxicity Testing ◽  
Antioxidant Potential ◽  
Gastric Ulcers ◽  
Albino Rats ◽  
Protective Effects ◽  
Sod Activity ◽  
Group I

Aim: The aim of this study is to evaluate the antioxidant properties and protective effects of aqueous anti-ulcer drug (AQAUD) against aspirin-induced gastric ulcer in albino rats. Methods: In this study, 30 male albino rats were divided into 5 groups of 6 each. Rats in group I served as normal control and received food and water. Animals in group II received food and water in addition to aspirin (400 mg/kg.b.wt) orally on the 14th day. Rats in groups III, IV and V received “AQAUD” (250 mg/kg.b.wt), (500 mg/kg.b.wt) and Omeprazole (20 mg/kg.b.wt) respectively for 14 days and aspirin (400 mg/kg.b.wt) orally on the 14th day. In vitro antioxidant property of “AQAUD” was assessed by its nitric oxide and hydroxyl radicals scavenging properties. The ulcer protective effect of “AQAUD” was assessed by determining the free and total acidity, ulcer index and % protection in the stomach content. The antioxidant potential in animals was evaluated by determining the concentrations of malondialdehyde and reduced glutathione. Superoxide dismutase and catalase activities were assayed in the stomach homogenates to further assess antioxidant potential. Total phenolics and flavonoid compounds were quantified to know the antioxidant content. Histopathological assessment of the gastric mucosa was used to assess the protective potentials of “AQAUD”. Data were analyzed using Statistical Package for Social Science (SPSS) version 21. Results: The results revealed that free acidity and ulcer indexes were significantly (p<0.05) reduced by “AQAUD”. There was a significant decrease in SOD activity of the stomach homogenates when compared to the aspirin group, with values for “AQAUD” 250 mg/kg.b.wt and “AQAUD” 500 mg/kg b.wt as 37.24±5.39ux10-2/mg protein and 23.64±2.91ux10-2/mg protein respectively. Result of acute toxicity testing showed that “AQAUD” is generally safe up to 5000 mg/kg b.wt. Conclusion: The results revealed that treatment with aspirin caused loss of gland architecture with erosion of epithelial layer, but AQAUD treatment ameliorated the effect of aspirin administration. The study revealed that “AQAUD” has considerable antioxidant potentials and can effectively protect against gastric ulcers.

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 Effects of Spirulina on Cyclophosphamide-Induced Ovarian Toxicity in Rats: Biochemical and Histomorphometric Evaluation of the Ovary

2013 ◽  
Vol 2013 ◽  
pp. 1-6 ◽  
Author(s):  
Nese Arzu Yener ◽  
Orhun Sinanoglu ◽  
Erdin Ilter ◽  
Aygen Celik ◽  
Gulbuz Sezgin ◽  
...  
Keyword(s):  
Single Dose ◽  
Control Group ◽  
Protective Effects ◽  
Primary Follicle ◽  
Sod Activity ◽  
Blue Green Algae ◽  
Group Iii ◽  
Ovarian Toxicity ◽  
Group I ◽  
Significant Difference

Cyclophosphamide (Cyc) is known to cause ovotoxicity and infertility in women. Our aim is to investigate the possible ovotoxic effects of Cyc and possible antioxidant and protective effects of blue-green algae, Spirulina (Sp), in rat ovaries. Eighteen rats were given: group I (n=6, control); group II (n=6, CP), a single dose Cyc; group III (n=6, Sp+Cyc), 7 days Sp+single dose Cyc. Tissue malondialdehyde (MDA) levels, superoxide dismutase (SOD), and catalase (CAT) activities are assessed biochemically. Normal and atretic primordial and primary follicle counts for all sections obtained for each ovary are calculated. Mean number of follicle counts for each group are compared. In Sp+Cyc group, tissue MDA levels were significantly lower than those in the CP and higher than those in the C group (CP>Sp+Cyc>C). Tissue SOD activity was significantly higher in Sp+Cyc group than that in the CP group and lower than that in the C group (C>Sp+Cyc>C). No statistically significant difference was found between the ovarian CAT activities in any group. Histomorphometrically, there was also no significant difference between the mean numbers of normal and atretic small follicle counts. Our results suggest that single dose Cyc has adverse effects on oxidant status of the ovaries and Sp has protective effects in Cyc-induced ovotoxicity.

scholarly journals Adalimumab Ameliorates Abdominal Aorta Cross Clamping Which Induced Liver Injury in Rats

2014 ◽  
Vol 2014 ◽  
pp. 1-8 ◽  
Author(s):  
Erkan Cure ◽  
Medine Cumhur Cure ◽  
Levent Tumkaya ◽  
Yildiray Kalkan ◽  
Ibrahim Aydin ◽  
...  
Keyword(s):  
Liver Injury ◽  
Abdominal Aorta ◽  
Liver Tissue ◽  
Cell Damage ◽  
Ischemia Reperfusion ◽  
Control Group ◽  
Albino Rats ◽  
Protective Effects ◽  
Necrosis Factor Alpha ◽  
Protein Levels

The aim of this study was to investigate the possible protective effects of adalimumab (ADA) on cell damage in rat liver tissue during ischemia/reperfusion (I/R) injury of infrarenal abdominal aorta. Thirty male Wistar-albino rats were divided into three groups: control, I/R, and I/R+ADA, each group containing 10 animals. Laparotomy without I/R injury was performed in the control group animals. Laparotomy in the I/R group was followed by two hours of infrarenal abdominal aortic cross ligation and then two hours of reperfusion. ADA (50 mg/kg) was administered intraperitoneally as a single dose, to the I/R+ADA group, five days before I/R. The tumor necrosis factor-alpha (TNF-α) (pg/mg protein) and nitric oxide (NO) (µmol/g protein) levels in the I/R group (430.8 ± 70.1, 8.0 ± 1.1, resp.) were significantly higher than those in the I/R+ADA group (338.0 ± 71.6,P=0.006; 6.3 ± 1.2,P=0.008) and the control group (345.5 ± 53.3,P=0.008; 6.5 ± 1.5,P=0.010, resp.). I/R causes severe histopathological injury to the liver tissue, but ADA leads to much less histopathological changes. ADA treatment significantly decreased the severity of liver I/R injury. ADA pretreatment may have protective effects on experimental liver injury.

scholarly journals Effects of Dexmedetomidine Postconditioning on Myocardial Ischemia/Reperfusion Injury in Diabetic Rats: Role of the PI3K/Akt-Dependent Signaling Pathway

2018 ◽  
Vol 2018 ◽  
pp. 1-10 ◽  
Author(s):  
Xiangyang Cheng ◽  
Jing Hu ◽  
Ya Wang ◽  
Hongwei Ye ◽  
Xiaohong Li ◽  
...  
Keyword(s):  
Myocardial Ischemia ◽  
Signaling Pathway ◽  
Ischemia Reperfusion Injury ◽  
Ischemia Reperfusion ◽  
Mrna Level ◽  
Diabetic Rats ◽  
Diabetic Rat ◽  
Protective Effects ◽  
Sod Activity ◽  
Group I

Objective. The present study was designed to determine whether dexmedetomidine (DEX) exerts cardioprotection against myocardial I/R injury in diabetic hearts and the mechanisms involved. Methods. A total of 30 diabetic rats induced by high-glucose-fat diet and streptozotocin (STZ) were randomly assigned to five groups: diabetic sham-operated group (DM-S), diabetic I/R group (DM-I/R), diabetic DEX group (DM-D), diabetic DEX + Wort group (DM-DW), and diabetic Wort group (DM-W). Another 12 age-matched male normal SD rats were randomly divided into two groups: sham-operated group (S) and I/R group (I/R). All rats were subjected to 30 min myocardial ischemia followed by 120 min reperfusion except sham groups. Plasmas were collected to measure the malondialdehyde (MDA), creatine kinase isoenzymes (CK-MB), and lactate dehydrogenase (LDH) levels and superoxide dismutase (SOD) activity at the end of reperfusion. Pathologic changes in myocardial tissues were observed by H-E staining. The total and phosphorylated form of Akt and GSK-3β protein expressions were measured by western blot. The ratio of Bcl-2/Bax at mRNA level was detected by reverse transcription-polymerase chain reaction (RT-PCR). Results. DEX significantly reduced plasma CK-MB, MDA concentration, and LDH level and increased SOD activity caused by I/R. The phosphorylation of Akt and GSK-3β was increased, Bcl-2 mRNA and the Bcl-2/Bax ratio was increased, and Bax mRNA was decreased in the DEX group as compared to the I/R group, while posttreatment with Wort attenuated the effects induced by DEX. Conclusion. The results of this study suggest that DEX postconditioning may increase the phosphorylation of GSK-3β by activating the PI3K/Akt signaling pathway and may inhibit apoptosis and oxidative stress of the myocardium, thus exerting protective effects in diabetic rat hearts suffering from I/R injury.

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