Ginkgo biloba inhibits bleomycin-induced lung fibrosis in rats

Iraz, Mustafa; Erdoğan, Hasan; Kotuk, Mahir; Yagmurca, Murat; Kılıç, Talat; Ermiş, Hilal; Fadıllıoğlu, Ersin; Yıldırım, Zeki

doi:10.1016/j.phrs.2005.12.009

Cited by 53 publications

(20 citation statements)

References 33 publications

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“…This was corroborated by a significant decrease in the number of PMNs and a decrease in hydroxyproline in the lung lavage fluid of rats pretreated with taurine compared to those not supplemented with taurine. Previously published data showed that the level of hydroxyproline was high on days 14 and 21 in lung tissue after bleomycin challenge in rats and mice [28][29][30]. Our data showed that hydroxyproline in BALF was the highest at day 7 and decreased by day 14 post bleomycin.…”

Section: Discussionsupporting

confidence: 65%

Protection of bleomycin-induced fibrosis and inflammation by taurine

Schuller‐Levis¹,

Gordon²,

Wang³

et al. 2009

International Immunopharmacology

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Section: Discussionsupporting

confidence: 65%

Protection of bleomycin-induced fibrosis and inflammation by taurine

Schuller‐Levis¹,

Gordon²,

Wang³

et al. 2009

International Immunopharmacology

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“…2). This data is consistent with previous studies indicating that a decrease in antioxidant activity following BLM treatment indicated the formation of ROS, which, in turn, caused further damage to lungs (20)(21)(22). However, an increase in the expression levels of Nrf2 (23) and Klf9 upon treatment with BLM has also been reported (24).…”

Section: Discussionsupporting

confidence: 92%

Involvement of Kruppel-like factor 9 in bleomycin-induced pulmonary toxicity

Wang

et al. 2015

Molecular Medicine Reports

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Abstract.Oxidative stress or the production of reactive oxygen species (ROS) has been implicated as an important factor in the development of bleomycin (BLM)-induced pulmonary toxicity; however, the mechanism behind the toxicity remains to be elucidated. The present study aimed to investigate the key factor involved in BLM-induced toxicity. The study was conducted in human pulmonary fibroblast (HPF) cells and in a mouse model. The ROS level, cell death assay, protein and gene expression levels of Kruppel-like factor 9 (Klf9) and other associated factors were assessed. A dose-dependent increase in ROS, lipid peroxidation, cell death, and protein and mRNA expression levels of NF-E2-related transcription factor 2 (Nrf2) and Klf9 were observed in BLM-treated cells. However, the expression levels of the other antioxidant proteins assessed, including catalase, super oxide dismutase, glutathione reductase and thioredoxin reductase 2, were decreased. The expression levels of Nrf2 were decreased in cells treated with a higher concentration (>200 µM) of BLM. These results suggested that in response to increased intracellular levels of ROS, above a critical threshold, Nrf2 stimulates the expression of Klf9, resulting in a further increase in Klf9-mediated ROS production and subsequent cell death. Furthermore, the data suggested that Klf9 may be considered as an adjunctive therapeutic target for BLM-induced pulmonary toxicity.

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“…Liu, 1992;J. Liu et al, 1993), Ginkgo biloba (Daba et al, 2002;Iraz et al, 2006), Moxibustion (R. Li et al, 2005), Fufang (Kong et al, 2005) etc. ), Immunosuppressants (Cyclosporin-A (Lossos, Or, Goldstein, Conner, & Breuer, 1996), Rapamycin analogue SDZ RAD (Simler et al, 2002)), Corticosteroids (Dexamethasone (F. Chen et al, 2006;Dik et al, 2003;H.…”

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

825

724

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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.

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Ginkgo biloba inhibits bleomycin-induced lung fibrosis in rats

Cited by 53 publications

References 33 publications

Protection of bleomycin-induced fibrosis and inflammation by taurine

Protection of bleomycin-induced fibrosis and inflammation by taurine

Involvement of Kruppel-like factor 9 in bleomycin-induced pulmonary toxicity

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

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