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Exp Lung Res ; 46(8): 297-307, 2020 10.
Artigo em Inglês | MEDLINE | ID: mdl-32748670

RESUMO

BACKGROUND: This study aims to explore the effect of thymoquinone (TQ) on particulate matter 2.5 (PM2.5)-induced lung injury. METHODS: The PM2.5 sample was provided by Shenyang Environment Monitor Central Station. Lung injury was established by intratracheal instillation PM2.5 (7.5 mg/kg) followed by TQ treatment (20 and 40 mg/kg) for 14 d in rats. Hematoxylin and eosin (HE) and Evans blue dye (EBD) staining were detected on lung tissues. ELISA, real-time PCR, western blotting and TUNEL assays were also performed. RESULTS: The data showed that TQ diminished lung injury and EBD accumulation. The number of macrophages, neutrophils, eosinophils, and lymphocytes was ameliorated after TQ treatment. In addition, TQ suppressed the inflammation reaction parameters (interleukin-1ß and -6, IL-1ß and IL-6; tumor necrosis factor-α, TNF-α) and oxidative stress in PM2.5-induced lung injury. The levels of nuclear factor erythroid 2-related factor 2 (Nrf2) and heme oxygenase (HO-1) were increased due to the treatment of TQ. The number of TUNEL-positive cells was prominently reduced in TQ-treated rats compared with that in PM2.5 group. Intratracheal instillation PM2.5 activated autophagy, whilst TQ blocked it in lung. CONCLUSIONS: Taken together, this study provides the first in vivo evidence that TQ suppresses inflammation, oxidative stress, apoptosis, and autophagy in PM2.5-induced lung injury.


Assuntos
Benzoquinonas/farmacologia , Lesão Pulmonar/induzido quimicamente , Lesão Pulmonar/tratamento farmacológico , Pulmão/efeitos dos fármacos , Material Particulado/efeitos adversos , Animais , Apoptose/efeitos dos fármacos , Autofagia/efeitos dos fármacos , Heme Oxigenase-1/metabolismo , Inflamação/induzido quimicamente , Inflamação/tratamento farmacológico , Inflamação/metabolismo , Pulmão/metabolismo , Lesão Pulmonar/metabolismo , Masculino , Fator 2 Relacionado a NF-E2/metabolismo , Estresse Oxidativo/efeitos dos fármacos , Ratos , Ratos Wistar , Transdução de Sinais/efeitos dos fármacos
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