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2017 ; 7
(1
): 3439
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Protective and therapeutic effect of felodipine against bleomycin-induced
pulmonary fibrosis in mice
#MMPMID28611390
Tanaka KI
; Niino T
; Ishihara T
; Takafuji A
; Takayama T
; Kanda Y
; Sugizaki T
; Tamura F
; Kurotsu S
; Kawahara M
; Mizushima T
Sci Rep
2017[Jun]; 7
(1
): 3439
PMID28611390
show ga
Idiopathic pulmonary fibrosis (IPF) involves alveolar epithelial injury and
abnormal collagen production caused by activated fibroblasts; transforming growth
factor (TGF)-?1 is implicated in this activation. In this study, we screened for
chemicals capable of inhibiting TGF-?1-induced collagen production in cultured
fibroblasts from medicines already in clinical use. We selected felodipine based
on its extent of collagen production inhibition, clinical safety profile, and
other pharmacological activity. Felodipine is a dihydropyridine Ca(2+) channel
blocker that has been used clinically to treat patients with high blood pressure.
Felodipine suppressed collagen production within LL29 cells in the presence of
TGF-?1, but not in its absence. Intratracheal administration of felodipine
prevented bleomycin-induced pulmonary fibrosis, alteration of lung mechanics and
respiratory dysfunction. Felodipine also improved pulmonary fibrosis, as well as
lung and respiratory function when administered after fibrosis development.
Furthermore, administration of felodipine suppressed a bleomycin-induced increase
in activated fibroblasts in the lung. We also found other dihydropyridine Ca(2+)
channel blockers (nifedipine and benidipine) inhibited collagen production in
vitro and partially prevented bleomycin-induced pulmonary fibrosis, alteration of
lung mechanics and respiratory dysfunction in vivo. We propose that these Ca(2+)
channel blockers may be therapeutically beneficial for IPF patients.
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