Oral N-acetylcysteine reduces bleomycin-induced lung damage and mucin Muc5ac expression in rats

Mata, M. M.; Ruı́z, Amparo; Cerdá, Miguel Jover; Martínez‐Losa, Magdalena; Cortijo, Julio; Santangelo, Francesco; Serrano-Mollar, Anna; Llombart‐Bosch, Antonio; Morcillo, Esteban J.

doi:10.1183/09031936.03.00018003

Cited by 79 publications

(52 citation statements)

References 29 publications

Supporting

Mentioning

Contrasting

Order By: Relevance

“…As a result of the injury, inflammation and cytokine dysregulation occur after BLM administration, fibroblasts are activated, and collagen production is stimulated, while collagen degradation is inhibited (Sleijfer 2001). In addition, several studies have demonstrated that bleomycin administration in rats decreases the antioxidative capacity, while increasing oxidative stress in the lung tissue (Mata et al 2003). …”

Section: Resultsmentioning

confidence: 99%

The antioxidant effect of boric acid and CoQ10 on pulmonary fibrosis in bleomycin induced rats

Çelikezen¹,

Oto²,

Özdemir³

et al. 2015

Bitlis Eren University Journal of Science and Technology

View full text Add to dashboard Cite

The purpose of this study is to investigate the antioxidant effects boric acid and CoQ10 has on pulmonary fibrosis in bleomycin induced rats. 32 wistar albino male rats were used in this study. The rats were categorised in four groups; a control group (only given normal saline), a bleomycin (BLM) group, a BLM + boric acid group, and a BLM + boric acid + CoQ10. The study period was adjusted to 30 days. Retinol, vitamin E, vitamin D, catalase, carbonic anhydrase, glucose, total protein, albumin, globulin, and total bilirubin levels were measured at the end of the study. There was a significant increase in the vitamin E levels of all groups (p<0.05). There was a statistically significant increase in the glucose level of all groups (P<0.001). There were significant decreases in albumin and total protein levels of all groups. While the significance level of the decrease in the albumin level was p<0.001, the significance level of the decrease in the total protein level was p<0.05. There was no significant difference in other biochemical parameters.

show abstract

Section: Resultsmentioning

confidence: 99%

The antioxidant effect of boric acid and CoQ10 on pulmonary fibrosis in bleomycin induced rats

Çelikezen¹,

Oto²,

Özdemir³

et al. 2015

Bitlis Eren University Journal of Science and Technology

View full text Add to dashboard Cite

show abstract

“…J. Wang, Giri, Hyde, Nakashima, & Javadi, 1990), Taurin (Blaisdell & Giri, 1995;Gurujeyalakshmi, Hollinger, & Giri, 1998;Gurujeyalakshmi, Iyer, Hollinger, & Giri, 1996;Gurujeyalakshmi, Wang, & Giri, 2000;Q. J. Wang, Giri, Hyde, & Nakashima, 1989), N-Acetylcysteine (Cortijo et al, 2001;Hagiwara, Ishii, & Kitamura, 2000;Mata et al, 2003;Serrano-Mollar et al, 2003;Shahzeidi, Sarnstrand, Jeffery, McAnulty, & Laurent, 1991;Yildirim et al, 2005), Vitamin E (Kilinc et al, 1993), Curcumin (Punithavathi, Venkatesan, & Babu, 2000), Aminoguanidine (X. L. Chen, Huang, Li, Wang, & Wang, 2001; X. L. Chen, Li, Zhou, Ai, & Huang, 2003;de Rezende, Martinez, Capelozzi, Simoes, & Beppu, 2000;Giri, Biring, Nguyen, Wang, & Hyde, 2002;Hu, Xu, & Li, 1999;Yildirim et al, 2004), Melatonin (Arslan, Zerin, Vural, & Coskun, 2002;Genovese, Di Paola et al, 2005;Yildirim et al, 2006), Bilirubin (H. D. , CAPE = caffeic acid phenethyl ester , Erdosteine (Boyaci et al, 2006;Sogut et al, 2004;Yildirim et al, 2005;Yildirim et al, 2004) etc. ), Angiotensin converting enzyme inhibitors (Captopril (R. Wang, Ibarra-Sunga, Verlinski, Pick, & Uhal, 2000), Ramipril (Marshall et al, 2004) etc.…”

Section: Drug Intervention Studies In the Bleomycin Modelmentioning

confidence: 99%

The bleomycin animal model: A useful tool to investigate treatment options for idiopathic pulmonary fibrosis?

Moeller

Ask

Warburton

et al. 2008

The International Journal of Biochemistry & Cell Biology

821

724

View full text Add to dashboard Cite

Different animal models of pulmonary fibrosis have been developed to investigate potential therapies for idiopathic pulmonary fibrosis (IPF). The most common is the bleomycin model in rodents (mouse, rat and hamster). Over the years, numerous agents have been shown to inhibit fibrosis in this model. However, to date none of these compounds are used in the clinical management of IPF and none has shown a comparable antifibrotic effect in humans. We performed a systematic review of publications on drug efficacy studies in the bleomycin model to evaluate the value of this model regarding transferability to clinical use. Between 1980 and 2006 we identified 246 experimental studies describing beneficial antifibrotic compounds in the bleomycin model. In 221 of the studies we found enough details about the timing of drug application to allow inter-study comparison. 211 of those used a preventive regimen (drug given ≤ day 7 after last bleomycin application), only 10 were therapeutic trials (> 7 days after last bleomycin application). It is critical to distinguish between drugs interfering with the inflammatory and early fibrogenic response from those preventing progression of fibrosis, the latter likely much more meaningful for clinical application. All potential antifibrotic compounds should be evaluated in the phase of established fibrosis rather than in the early period of bleomycin-induced inflammation for assessment of its antifibrotic properties. Further care should be taken in extrapolation of drugs successfully tested in the bleomycin model due to partial reversibility of bleomycin induced fibrosis over time. The use of alternative and more robust animal models, which better reflect human IPF, is warranted.

show abstract

“…As an alternative, NAC has been shown to improve glutathione homeostasis by increasing cysteine levels, the ratelimiting substrate in glutathione synthesis. Notably, NAC significantly decreases primary inflammatory reactions, collagen deposition, and the progression of bleomycin-induced lung fibrosis (55)(56)(57). NAC, however, also has prooxidant characteristics, and there are studies suggesting that NAC does not necessarily improve lung glutathione homeostasis (53,54).…”

Section: Exogenous Antioxidants and Antioxidant Mimetics In Pulmonarymentioning

confidence: 99%

Oxidative Stress in Pulmonary Fibrosis

Kinnula

Fattman

Tan

et al. 2005

Am J Respir Crit Care Med

369

132

View full text Add to dashboard Cite

Idiopathic ulmonary fibrosis (histopathology of usual interstitial pneumonia) is a progressive lung disease of unknown etiology. No treatment has been shown to improve the prognosis of the patients with this disease. Recent evidence, including the observations that the patients with idiopathic pulmonary fibrosis have higher levels of oxidant stress than control patients, and a recent multicenter European study examining the effect of the antioxidant N-acetylcysteine on the progression of idiopathic pulmonary fibrosis suggest that the cellular redox state may play a significant role in the progression of this disease. These complex mechanisms include activation of growth factors as well as regulation of matrix metalloproteinases and protease inhibitors. Potential future approaches for the therapy of interstitial pulmonary fibrosis may involve synthetic agents able to modulate cellular redox state. Investigation into therapeutic approaches to inhibit oxidant-mediated reactions in the initiation and progression of pulmonary fibrosis may provide hope for the future treatment of this disease.Keywords: antioxidant; idiopathic pulmonary fibrosis; oxidant; radical Idiopathic pulmonary fibrosis (IPF) is a prototype of idiopathic interstitial pneumonias, a chronic disease of the lung parenchyma that leads to diffuse scarring and end-stage tissue fibrosis (1). Typical features in this disease include dyspnea, diffuse interstitial infiltrates, progressive lung fibrosis, and poor prognosis. The pathologic changes in IPF include patchy fibrotic lesions that vary both in age and activity, and only weak inflammation. The focal zones of fibroblast proliferation are called "fibroblastic foci" and appear to occur at sites of recent alveolar injury (1, 2). The biochemical mechanisms in the pathogenesis of IPF are still poorly understood and medical therapies have thus far offered little if any benefit against the progression of this disease (1,3,4).As the name implies, there is no known etiologic stimulus that initiates this disease. Current evidence suggests that both endogenous and exogenous stimuli may injure the alveolar epithelium. This is followed by an abnormal repair process in individuals unable to effectively heal the damage. The majority of the original articles and reviews on IPF have focused on the (Received in original form January 5, 2005; accepted in final form May 3, 2005) This and the original studies of V.L.K.

show abstract

Oral N-acetylcysteine reduces bleomycin-induced lung damage and mucin Muc5ac expression in rats

Cited by 79 publications

References 29 publications

The antioxidant effect of boric acid and CoQ10 on pulmonary fibrosis in bleomycin induced rats

The antioxidant effect of boric acid and CoQ10 on pulmonary fibrosis in bleomycin induced rats

The bleomycin animal model: A useful tool to investigate treatment options for idiopathic pulmonary fibrosis?

Oxidative Stress in Pulmonary Fibrosis

Contact Info

Product

Resources

About