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Carvedilol attenuates experimentally induced silicosis in rats via modulation of P-AKT/mTOR/TGFβ1 signaling.

Abstract：

:Silicosis is a well acknowledged occupational lung disorder with considerable negative impact on the patients' quality of life. Various signaling pathways have been reported to interplay in the pathogenesis of pulmonary fibro-proliferative disorders; of which, P-AKT/mTOR signaling pathway. The current study highlights the potential pulmonary protective effect of carvedilol; a non-selective α/β blocker against experimental silicosis-induced in rats by the intranasal installation of silica (50 mg/rat, 1 ml 0.9% NaCl). Carvedilol (20 mg/kg, orally) was administered for 8 weeks post intranasal silica installation. Carvedilol significantly attenuated silica-induced pulmonary damage on all the investigated scales. Inflammatory, oxidative/anti-oxidative and fibrotic incidences significantly improved with a significant histopathological restoration of lung architecture and attenuation of inflammatory and fibrotic biomarkers expression. Carvedilol significantly reduced lung contents of P-AKT and mTOR which, appears to be the main mechanism underlying the pulmonary protective effect of carvedilol. In conclusion; carvedilol attenuated silica-induced pulmonary fibrosis by modulating P-AKT/mTOR/TGFβ1 signaling and underlying inflammatory and fibrotic sequel.

journal_name

Int Immunopharmacol

journal_title

International immunopharmacology

authors

Helal MG,Said E

doi

10.1016/j.intimp.2019.02.011

subject

Has Abstract

pub_date

2019-05-01 00:00:00

pages

47-55

eissn

1567-5769

issn

1878-1705

pii

S1567-5769(18)31251-7

journal_volume

70

pub_type

杂志文章

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