The effects of erdosteine on lung injury induced by the ischemia-reperfusion of the hind-limbs in rats (original) (raw)
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Biological Trace Element Research, 2007
The aim of this study was to investigate the protective effects of erdosteine and vitamins C and E (VCE) on the lungs after performing hind limb ischemia-reperfusion (I/R) by assessing oxidative stress, plasma copper (Cu), and zinc (Zn) analysis. The animals were divided randomly into four groups as nine rats each as follows: control, I/R, I/R plus erdosteine, and I/R plus VCE combination. I/R period for 60 min was performed on the both hind limbs of all the rats in the groups of I/R, erdosteine with I/R, VCE with I/R allowing 120 min of reperfusion. The animals received orally erdosteine one time in a day and 3 days before I/R in the erdosteine group. In the VCE group, the animals VCE combination received one time in a day and 3 days before I/R, although placebo was given to control and I/R group animals. Lung lipid peroxidation (malondialdehyde [MDA]) level, superoxide dismutase (SOD), and catalase activities were increased, although lung glutathione (GSH) and plasma Zn levels decreased in I/R group in lung tissue compared with the control group. Serum MDA level, creatine kinase, and lactate dehydrogenase activities were increased in I/R group compared with the control. Lung MDA and plasma Zn levels and lung SOD activity were decreased by erdosteine administration, whereas lung GSH levels after I/R increased. The plasma Zn levels and lung SOD activity were decreased by VCE administration, although the plasma Cu and lung GSH levels increased after I/R. In conclusion, erdosteine has an antioxidant role on the values in the rat model, and it has more protective affect than in VCE in attenuating I/R-induced lung injury in rats.
Hypobaric-hypoxia-induced pulmonary damage in rats ameliorated by antioxidant erdosteine
Acta Histochemica, 2006
Free radical-mediated injury to lung and pulmonary vasculature is an important mechanism in hypoxia-induced lung damage. In this study, we aimed to investigate the potential protective effects of erdosteine as an antioxidant agent on hypobaric hypoxia-induced pulmonary hypertension. Adult male rats were assigned randomly to three groups. The first group of rats was exposed to hypobaric-hypoxia and the second group was treated with erdosteine (20 mg/kg, daily) for 2 weeks, during which time they were in a hypoxic chamber. These groups were compared with normoxic controls. All rats were sacrificed after 2 weeks. The hypoxia-induced increase in right ventricle to left ventricle plus septum weight ratio (from 0.2070.01 to 0.2670.01) was reduced significantly in the erdosteine-treated group (0.2370.01). Malondialdehyde levels were elevated (from 0.3370.11 to 0.5970.02) and total antioxidant status was not changed significantly (from 1.7770.42 to 2.6170.23) by hypoxia. In contrast to the hypoxia-exposed group, malondialdehyde levels were significantly decreased in the erdosteine-treated group (0.3770.02). Total antioxidant status (4.0370.22) was significantly higher in erdosteine-treated rats when compared to non-treated rats. Histopathological examination demonstrated that erdosteine prevented inflammation and protected lung parenchyma and pulmonary endothelium of hypoxia-exposed rats.
The effect of erdosteine on ischemia-reperfusion injury in skeletal muscle of rats
Annals of Clinical and Analytical Medicine
Aim: As a mucolytic agent, Erdosteine has two sulfhydryl groups. These groups function as free radical scavengers, which has protective effects against ischemia-reperfusion (IR) injury. In this study, we aimed to observe the effects of erdosteine on skeletal muscle tissue in a rat lower extremity IR injury model. Material and Methods: A total of 18 Wistar albino rats were separated into 3 groups (n: 6); Control group (C), IR group (IR) and IR group with erdosteine (IR-E). Erdosteine administered intraperitoneally (150 mg.kg-1). Rat tissues were taken for histopathological and immunohistochemical evaluations after 2 hours of ischemia and 2 hours of reperfusion period. Results: Blood flow measurements were significantly higher in the IR-E group than in the IR group. In the IR group, endothelial caspase 3 and 8 enzyme expression was significantly higher than C and IR-E groups. Muscle caspase 3 enzyme expression was higher in the IR group than C and IR-E groups. IR and IR-E groups showed increased inflammation, vascular congestion and myositis injury levels than the C group. Also, inflammation, vascular congestion and myositis injury showed a significant decrease in the IR-E group than IR group. Discussion: As a result, erdosteine has a protective effect against skeletal tissue damage resulting from IR injury in rats. The results show the possibility of clinical administration of erdosteine for I/R injury of skeletal muscle tissue.
Journal of Applied Toxicology, 2006
This study was carried out to investigate comparatively the frequency of apoptosis in lung epithelial cells after intratracheal instillation of endotoxin [lipopolysaccharide (LPS)] in rats and the role of tumor necrosis factor alpha (TNF-α α α α α) on apoptosis, and the effects of erdosteine and N-acetylcysteine on the regulation of apoptosis. Female Wistar rats were given oral erdosteine (10-500 mg kg − − − − −1) or N-acetylcysteine (10-500 mg kg − − − − −1) once a day for 3 consecutive days. Then the rats were intratracheally instilled with LPS (5 mg kg − − − − −1) to induce acute lung injury. The rats were killed at 24 h after LPS administration. Lung tissue samples were stained with hematoxylin-eosin for histopathological assessments. The apoptosis level in the lung bronchial and bronchiolar epithelium was determined using the TUNEL (terminal deoxynucleotidyl transferase-mediated dUTP nick endlabelling) method. Cytoplasmic TNF-α α α α α was evaluated by immunohistochemistry. Pretreatment with erdosteine and pretreatment with N-acetylcysteine at a dose of 10 mg kg − − − − −1 had no protective effect on LPS-induced lung injury. When the doses of drugs increased, the severity of the lung damage caused by LPS decreased. It was found that as the pretreatment dose of erdosteine was increased, the rate of apoptosis induced by LPS in lung epithelial cells decreased and this decrease was statistically significant in doses of 300 mg kg − − − − −1 and 500 mg kg − − − − −1. Pretreatment with N-acetylcysteine up to a dose of 500 mg kg − − − − −1 did not show any significant effect on apoptosis regulation. It was noticed that both antioxidants had no significant effect on the local production level of TNF-α α α α α. These findings suggest that erdosteine could be a possible therapeutic agent for acute lethal lung injury and its mortality.
Diethylmaleate, a pro-oxidant, attenuates experimental ischaemia-reperfusion-induced lung injury
British Journal of Surgery, 2002
Background:Systemic ischaemia–reperfusion (IR) injury is in part an oxidant injury mediated by neutrophils. Diethylmaleate (DEM), an intracellular pro-oxidant agent, has been shown to alleviate neutrophil-mediated tissue injury. The aim of this study was to evaluate whether DEM could have a protective effect on neutrophil-mediated lung injury in an animal model of lower-torso IR.Systemic ischaemia–reperfusion (IR) injury is in part an oxidant injury mediated by neutrophils. Diethylmaleate (DEM), an intracellular pro-oxidant agent, has been shown to alleviate neutrophil-mediated tissue injury. The aim of this study was to evaluate whether DEM could have a protective effect on neutrophil-mediated lung injury in an animal model of lower-torso IR.Methods:Sprague–Dawley rats (seven per group) were randomized into three groups. The control group underwent midline laparotomy only; the IR group underwent laparotomy and clamping of the infrarenal abdominal aorta for 30 min followed by 2 h of reperfusion; and the third group was pretreated with DEM 6 mmol/kg intraperitoneally 1 h before the IR insult.Sprague–Dawley rats (seven per group) were randomized into three groups. The control group underwent midline laparotomy only; the IR group underwent laparotomy and clamping of the infrarenal abdominal aorta for 30 min followed by 2 h of reperfusion; and the third group was pretreated with DEM 6 mmol/kg intraperitoneally 1 h before the IR insult.Results:IR resulted in a significant increase in both microvascular leakage and pulmonary neutrophil infiltration as measured by bronchoalveolar lavage protein concentration and pulmonary myeloperoxidase activity respectively. Pretreatment with DEM significantly attenuated both microvascular leakage and neutrophil infiltration.IR resulted in a significant increase in both microvascular leakage and pulmonary neutrophil infiltration as measured by bronchoalveolar lavage protein concentration and pulmonary myeloperoxidase activity respectively. Pretreatment with DEM significantly attenuated both microvascular leakage and neutrophil infiltration.Conclusion:Preconditioning with DEM protected against IR-induced lung injury. This protective effect raises the possibility of using pro-oxidants to prevent inflammatory injury. © 2002 British Journal of Surgery Society LtdPreconditioning with DEM protected against IR-induced lung injury. This protective effect raises the possibility of using pro-oxidants to prevent inflammatory injury. © 2002 British Journal of Surgery Society Ltd
Erdosteine ameliorates the harmful effects of ischemia-reperfusion injury on the liver of rats
Acta cirurgica brasileira, 2017
To investigate the potential protective effects of erdosteine against the harmful effects of ischemia-reperfusion injury on the liver in an experimental rat model. Forty rats were divided into 4 groups. In the sham group, only the hepatic pedicle was mobilized. No other manipulation or treatment was performed. In the other groups, ischemia was achieved by clamping the hepatic pedicle for 60 min. After that, 90 min reperfusion was provided. In the control group, no treatment was given. In the perioperative treatment group, 100 mg/kg erdosteine was administered 2 hours before ischemia induction. In the preoperative treatment group, 100 mg/kg/day erdosteine was administered daily for ten days before the operation. At the end of the procedures, blood and liver samples were obtained for biochemical and histopathological assessment. Treatment with erdosteine ameliorated the histopathological abnormalities when compared with the control group. Furthermore, this treatment significantly decr...
Effects of Erdosteine in Experimental Sepsis Model in Rats
Hong Kong Journal of Emergency Medicine, 2011
Objective Erdosteine is a mucolytic agent that is known to possess antioxidant effects. This study investigated the effects of erdosteine on endothelin-1 (ET-1) levels and oxidative stress parameters superoxide dismutase (SOD) and malondialdehyde (MDA) in a rat sepsis model. Methods Four groups of Wistar albino rats (n=8 per group) were randomly allocated to the following groups: sham (group 1), sepsis (group 2), erdosteine control (group 3) and a sepsis group pretreated with erdosteine (group 4). Sepsis was induced using E. Coli ATCC 25922 inoculation. Serum ET-1, liver tissue SOD and MDA levels were determined in all groups. Results ET-1 levels were significantly higher in group 2 compared to groups 1, 3 and 4 (p<0.001, p=0.002 and p<0.001, respectively). Similarly, MDA levels in groups 1, 3 and 4 were significantly lower relative to group 2 (p<0.001, p=0.022 and p=0.010, respectively). Additionally, SOD activities in these same three groups were found to be significantly...
The protective effect of erdosteine on short-term global brain ischemia/reperfusion injury in rats
Progress in Neuro-Psychopharmacology and Biological Psychiatry, 2009
Experimental studies have demonstrated that free radicals play a major role on neuronal injury during ischemia/reperfusion (I/R) in rats. Erdosteine is a thioderivative endowed with mucokinetic, mucolytic and free-radical-scavenging properties. The aim of the present study was to investigate the effect of erdosteine treatment against short-term global brain ischemia/reperfusion injury in rats. The study was carried out on Wistar rats divided into four groups. (i) Control group, (ii) ischemia/reperfusion group, (iii) ischemia/reperfusion + erdosteine group, and (iv) erdosteine group. Superoxide dismutase (SOD), catalase (CAT), and glutathione peroxidase (GSH-Px) activities as well as thiobarbituric acid reactive substances (TBARSs) and nitric oxide (NO) levels were analysed in erythrocyte and plasma of rats. Plasma NO levels were significantly higher in the ischemia/reperfusion group than the other groups. The activities of SOD and GSH-Px were decreased, while TBARS levels increased in the ischemia/reperfusion group compared to other groups in both plasma and erythrocyte. The erythrocyte CAT activity was higher in erdosteine group and there was a statistically significant increase, when compared with the erdosteine plus ischemia/reperfusion group. By treating the rats with erdosteine, the depletion of endogenous antioxidant enzymes (SOD, CAT, GSH-Px) and increase of TBARS and NO levels were prevented. This study, therefore, suggests that erdosteine reduces parameters of oxidative stress is well supported by the data.
Journal of Surgical …, 2008
Background. The aim of this study was to clarify whether levosimendan could prevent lung tissue injury from limb ischemia/reperfusion. Methods. The common femoral arteries of 50 New Zealand white rabbits, both male and female, each weighing about 3 kg, were clamped and 1 h of ischemia followed by 4 h of reperfusion. In an attempt to decrease reperfusion injury, the rabbits were given levosimendan in Group A. In Group B, iloprost was infused at the same period. A similar value of saline solution was given in the control group, Group C correspondingly. Levosimendan and iloprost were given together the Group E, and Group D was sham group without medication and ischemia. Blood pH, pO2, pCO2, HCO3, Na, K, creatine phosphokinase, lactate dehydrogenase values were determined at the end of the reperfusion period. Malondialdehyde (MDA) was measured in plasma and lung as an indicator of free radicals. Hemodynamics parameters were noted for each group. After the procedure, left lung tissues were taken for histopathologic study. Results. Blood PO2 and HCO3 levels were significantly higher (P < 0.05) and creatine phosphokinase, lactate dehydrogenase, and MDA levels were significantly lower (P < 0.05) in Groups A, B, D, and E compared with Group C. Similarly, the MDA levels in the lung tissue and plasma levels were significantly lower in the treatment groups compared with the control group (P < 0.05). Lung damage was significantly higher in Group C. There was no significant difference between groups in other parameters. Conclusions. The results suggest that levosimendan and iloprost are useful for attenuating oxidative lung damage occurring after a period of limb ischemia/reperfusion.