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Life Sci ; 309: 120988, 2022 Nov 15.
Artigo em Inglês | MEDLINE | ID: mdl-36155181

RESUMO

AIMS: Pulmonary fibrosis (PF) is considered as an end stage for many lung diseases. Mesenchymal stem cells (MSC) as regenerative therapy have become a remarkably valuable therapeutic strategy in different diseases. Hydrogen sulfide has been recently introduced into the medical field for its antifibrotic properties in addition to enhancement of MSC stemness and function. The aim of the present study was to investigate the ability of BM-MSC in combination with NaHS to attenuate Bleomycin induced pulmonary fibrosis was studied in rats. A special emphasis was given to miR-21 and GAS5 as important players in the development of PF. MAIN METHODS: PF was induced in 32 Wistar male rats by single endotracheal injection of bleomycin, those were randomly divided into four groups (8 rats each): (untreated PF group) - (PF + MSC) treated group- (PF + NaHS treated group) - PF + combined (NAHS + MSC) treated group. KEY FINDINGS: Induction of PF was associated with increased miR-21 and decreased lncRNA-GAS5 expression. Treatment with either NaHS or BM-MSC leads to an inhibitory effect on pulmonary fibrosis as evidenced by improvement of histopathological studies, pulmonary function tests, reduction of inflammatory and fibrotic markers like Hydroxyproline, TNF α, TGF-ß and caspase -3 together with downregulation miR-21 and increase lncRNA-GAS5 expression. SIGNIFICANCE: The current work revealed the inhibitory effect of combined NaHS and BM-MSC on pulmonary fibrosis with concomitant modulation of miR-21 and lncRNA-GAS5 expression.


Assuntos
Sulfeto de Hidrogênio , Células-Tronco Mesenquimais , MicroRNAs , Fibrose Pulmonar , RNA Longo não Codificante , Animais , Masculino , Ratos , Bleomicina , Medula Óssea/metabolismo , Caspases/metabolismo , Sulfeto de Hidrogênio/metabolismo , Hidroxiprolina/metabolismo , MicroRNAs/genética , MicroRNAs/metabolismo , Fibrose Pulmonar/induzido quimicamente , Fibrose Pulmonar/genética , Fibrose Pulmonar/terapia , Ratos Wistar , RNA Longo não Codificante/metabolismo , Fator de Crescimento Transformador beta/metabolismo , Fator de Necrose Tumoral alfa/metabolismo
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