FTS reduces bleomycin-induced cytokine and chemokine production and inhibits pulmonary fibrosis in mice

Yara, Satomi; Kawakami, Kazuyoshi; Kudeken, Norifumi; Tohyama, Masaki; Teruya, Koji; Chinen, T.; Awaya, Akira; Saitô, Atsushi

doi:10.1046/j.1365-2249.2001.01493.x

Cited by 51 publications

(34 citation statements)

References 23 publications

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“…TNF-α functions as a chemokine in inflammatory cells, in addition to promoting the synthesis of fibronectin, prostaglandin and TGF-β. Depletion of TNF-α by antibodies has demonstrated a beneficial effect in the inhibition of bleomycin-induced lung injury (28,29). In the present study, a marked increase in TNF-α levels in the lungs occurred following bleomycin exposure, which was suppressed by apigenin treatment in a dose-dependent manner (Fig.…”

Section: A B a B Csupporting

confidence: 62%

Apigenin protects against bleomycin-induced lung fibrosis in rats

Chen

Zhao

2015

Experimental and Therapeutic Medicine

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Abstract. Apigenin is a non-toxic and non-mutagenic flavone that exists abundantly in numerous herbs and vegetables. Apigenin exerts anti-proliferative and anti-inflammatory properties. The aim of the present study was to investigate the effects of apigenin on bleomycin-induced lung fibrosis in rats. A single intratracheal instillation of bleomycin (5 mg/kg) was administered and rats were sacrificed on 7 and 28 days post bleomycin instillation. The instillation of bleomycin resulted in decreased body weight and an increase in the lung index. In addition, bleomycin administration increased the hydroxyproline content, myeloperoxidase (MPO) activity, tumor necrosis factor (TNF)-α and transforming growth factor (TGF)-β levels and decreased the superoxide dismutase (SOD) activity in the rat lung tissues. Excessive collagen deposits were detected in the lung tissues in bleomycin-treated rats compared with normal control rats. Notably, the oral administration of apigenin (10, 15 and 20 mg/kg/day) appeared to prevent the fibrotic process. The treatment suppressed the increases in hydroxyproline content, MPO activity, TNF-α and TGF-β levels and attenuated the reduction of SOD activity that were induced by bleomycin. Furthermore, excessive collagen deposition was inhibited by the apigenin treatment. Collectively, these results suggest that apigenin may function as a potent anti-inflammatory and anti-fibrotic agent against bleomycin-induced lung fibrosis.

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Section: A B a B Csupporting

confidence: 62%

Apigenin protects against bleomycin-induced lung fibrosis in rats

Chen

Zhao

2015

Experimental and Therapeutic Medicine

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“…Facteur thymique serique early (Yara et al, 2001) 19 5 rhIL-1 beta early (M. Yasui et al, 1991) 19 6 APC early (H. Yasui et al, 2001) 19 7 CD36 early (Yehualaeshet et al, 2000) 19 8 KGF early (Yi et al, 1996) 19 9…”

Section: Idmentioning

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

841

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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“…Researchers have reported that several drugs, including macrolide compounds, 24) thymic hormone, 25) and herbal compounds, 26) have anti-fibrotic actions in the experimental animal models of pulmonary fibrosis. The mechanisms underlying the anti-fibrotic actions of these drugs on lung fibroblasts are yet to be determined.…”

Section: Resultsmentioning

confidence: 99%

Efficient Delivery to Human Lung Fibroblasts (WI-38) of Pirfenidone Incorporated into Liposomes Modified with Truncated Basic Fibroblast Growth Factor and Its Inhibitory Effect on Collagen Synthesis in Idiopathic Pulmonary Fibrosis

Togami

Miyao

Miyakoshi

et al. 2015

Biological & Pharmaceutical Bulletin

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In the present in vitro study, we assessed the delivery of pirfenidone incorporated into liposomes modified with truncated basic fibroblast growth factor (tbFGF) to lung fibroblasts and investigated the antifibrotic effect of the drug. The tbFGF peptide, KRTGQYKLC, was used to modify the surface of liposomes (tbFGF-liposomes). We used the thin-layer evaporation method, followed by sonication, to prepare tbFGFliposomes containing pirfenidone. The cellular accumulation of tbFGF-liposomes was 1.7-fold greater than that of non-modified liposomes in WI-38 cells used as a model of lung fibroblasts. Confocal laser scanning microscopy showed that tbFGF-liposomes were widely localized in WI-38 cells. The inhibitory effects of pirfenidone incorporated into tbFGF-liposomes on transforming growth factor-β1 (TGF-β1)-induced collagen synthesis in WI-38 cells were evaluated by measuring the level of intracellular hydroxyproline, a major component of the protein collagen. Pirfenidone incorporated into tbFGF-liposomes at concentrations of 10, 30, and 100 µM significantly decreased the TGF-β1-induced hydroxyproline content in WI-38 cells. The antifibrotic effect of pirfenidone incorporated into tbFGF-liposomes was enhanced compared with that of pirfenidone solution. These results indicate that tbFGF-liposomes are a useful drug delivery system of anti-fibrotic drugs to lung fibroblasts for the treatment of idiopathic pulmonary fibrosis.

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FTS reduces bleomycin-induced cytokine and chemokine production and inhibits pulmonary fibrosis in mice

Cited by 51 publications

References 23 publications

Apigenin protects against bleomycin-induced lung fibrosis in rats

Apigenin protects against bleomycin-induced lung fibrosis in rats

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

Efficient Delivery to Human Lung Fibroblasts (WI-38) of Pirfenidone Incorporated into Liposomes Modified with Truncated Basic Fibroblast Growth Factor and Its Inhibitory Effect on Collagen Synthesis in Idiopathic Pulmonary Fibrosis

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