Hypobaric-hypoxia-induced pulmonary damage in rats ameliorated by antioxidant erdosteine

Uzun, Orhan; Balbay, Öner; Çomunogˇlu, Nil Üstündagˇ; Yavuz, Özlem; Annakkaya, Ali Nihat; Güler, Selver; Silan, Coşkun; Erbaş, Mete; Arbak, Peri

doi:10.1016/j.acthis.2006.01.001

Cited by 20 publications

(19 citation statements)

References 37 publications

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“…Erdosteine inhibits the XO activity and by this way might decrease the I/R injury. Beneficial effect of erdosteine as an antioxidant against the I/R toxicity in rats has been shown [28,29]. The statistically significant reduced XO and MDA levels have been noted in our study groups with erdosteine compared to the I/R group.…”

Section: Discussionsupporting

confidence: 50%

Combination antioxidant effect of α-tocoferol and erdosteine in ischemia–reperfusion injury in rat model

et al. 2009

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The erdosteine and α-tocoferol significantly reversed the effect of protein oxidation and lipid peroxidation induced by I/R shown by the decreased levels of MDA and XO activities. Both MDA and XO levels were found to be lower in group 6 compared to single agent treatment groups, and this was significantly different. All treatment groups showed increased SOD activity, which accounts for their oxidative properties. The mean Paller score of the combination treatment group (group 6) was lower than all groups except the sham group (3.67 ± 1.2), and this finding was statistically significant (0.05). Our results showed that the antioxidant pretreatment with α-tocopherol and erdosteine combination reduced lipid peroxidation of renal cellular membranes in a model of normothermic renal ischemia-reperfusion in rats. Combination of erdosteine and α-tocopherol has a synergistic effect of protection against oxidative processes. Long-term use of α-tocopherol seems to have a greater effect on the prevention of IR injury. However, further investigations are needed for the clinical applications of our findings.

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Section: Discussionsupporting

confidence: 50%

Combination antioxidant effect of α-tocoferol and erdosteine in ischemia–reperfusion injury in rat model

et al. 2009

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“…After oral administration of 300 mg, the peak plasma concentration of erdosteine, 1.26 ± 0.23 μg/ml, is reached 1.18 ± 0.26 h after administration [10]. In our experiments, LPS-induced IkBα degradation was attenuated by 10 μg/ml of erdosteine, but not 1 μg/ml of erdosteine.…”

Section: Discussionsupporting

confidence: 49%

“…In addition, erdosteine reduced hemorrhagic shock-induced acute lung injury [9] and hypoxia-induced pulmonary damage in animal models [10]. However, little is known about the detailed mechanisms of the anti-inflammatory effect of erdosteine.…”

Section: Introductionmentioning

confidence: 99%

Anti-inflammatory Effect of Erdosteine in Lipopolysaccharide-Stimulated RAW 264.7 Cells

et al. 2016

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Erdosteine is widely used as a mucolytic agent and also has free radical scavenging and antioxidant activities. However, little is known about the mechanisms of the anti-inflammatory effect of erdosteine. We investigated the effect of erdosteine on the activation of the nuclear factor (NF)-kB/inhibitor of NFkB (IkB), and the mitogen-activated protein kinase (MAPK) and Akt pathways in the mouse macrophage cell line RAW 264.7. Cultured RAW 264.7 cells were pretreated with erdosteine and stimulated with lipopolysaccharide (LPS). In Western blotting, pretreatment with erdosteine inhibited the IkBα degradation induced in RAW 264.7 cells by LPS. LPS-induced IkB kinase (IKK) activity and NF-kB transcription were inhibited by pretreatment with erdosteine. Production of IL-6 and IL-1β was also inhibited by erdosteine pretreatment. However, erdosteine did not inhibit LPS-induced phosphorylation of Akt and MAPKs. These results suggest that the anti-inflammatory effect of erdosteine in mouse macrophages is mediated through inhibition of LPS-induced NF-kB activation.

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“…In rats, compounds with antioxidant activities have been found to inhibit pulmonary hypertension and/or right ventricular dysfunction. Such compounds include probucol (19), N-acetylcysteine (16,23), tempol (9,20), erdosteine (46), allicin (43), pyrrolidine dithiocarbamate (17,39), superoxide dismutase (22), allopurinol (20), sulfur dioxide (21), resveratrol (7,52), and EUK-134 (35). In neonatal lambs with persistent pulmonary hypertension, superoxide dismutase was found to improve oxygenation, reduce oxidation (24), restore endothelial nitric oxide synthase expression and function (10), and normalize phosphodiesterase 5 (11).…”

Section: Evidence For Beneficial Effects Of Antioxidants In Animal Momentioning

confidence: 99%

Reactive Oxygen Species and Antioxidants in Pulmonary Hypertension

Wong

Bansal

Pavlickova

et al. 2013

Antioxidants & Redox Signaling

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Significance: Pulmonary hypertension is a devastating disorder without any available treatment strategies that satisfactorily promote the survival of patients. The identification of new therapeutic strategies to treat patients with pulmonary hypertension is warranted. Recent Advances: Human studies have provided evidence that there is increased oxidative stress (lipid peroxidation, protein oxidation, DNA oxidation, and the depletion of smallmolecule antioxidants) in patients with pulmonary hypertension. A variety of compounds with antioxidant properties have been shown to have beneficial therapeutic effects in animal models of pulmonary hypertension, possibly supporting the hypothesis that reactive oxygen species (ROS) are involved in the progression of pulmonary hypertension. Thus, understanding the molecular mechanisms of ROS actions could contribute to the development of optimal, antioxidant-based therapy for human pulmonary hypertension. One such mechanism includes action as a second messenger during cell-signaling events, leading to the growth of pulmonary vascular cells and right ventricular cells. Critical Issues: The molecular mechanisms behind promotion of cell signaling for pulmonary vascular cell growth and right ventricular hypertrophy by ROS are not well understood. Evidence suggests that iron-catalyzed protein carbonylation may be involved. Future Directions: Understanding precise mechanisms of ROS actions should be useful for designing preclinical animal experiments and human clinical trials of the use of antioxidants and/or other redox compounds in the treatment of pulmonary hypertension.

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Hypobaric-hypoxia-induced pulmonary damage in rats ameliorated by antioxidant erdosteine

Cited by 20 publications

References 37 publications

Combination antioxidant effect of α-tocoferol and erdosteine in ischemia–reperfusion injury in rat model

Combination antioxidant effect of α-tocoferol and erdosteine in ischemia–reperfusion injury in rat model

Anti-inflammatory Effect of Erdosteine in Lipopolysaccharide-Stimulated RAW 264.7 Cells

Reactive Oxygen Species and Antioxidants in Pulmonary Hypertension

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